{"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"DRP000042","sample_accession":"DRS000065","experiment_accession":"DRX000066","run_accession":"DRR000152","run_center_name":"UT-MGS","machine_type":"Illumina Genome Analyzer","paired_end":false,"study_title":"Comprehensive identification and characterization of the binding sites of STAT6 in STAT6 overexpressed BEAS-2B cells","study_abstract":"Comprehensive identification and characterization of the binding sites of STAT6 in STAT6 overexpressed BEAS-2B cells. We used ChIP-Seq method, in which next gene sequencing technology and chromatin-immunoprecipitation assay were combined.","study_primary_id":"DRP000042"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"DRP000043","sample_accession":"DRS000066","experiment_accession":"DRX000067","run_accession":"DRR000153","run_center_name":"UT-MGS","machine_type":"Illumina Genome Analyzer","paired_end":false,"study_title":"Comprehensive identification and characterization of the binding sites of STAT6 in STAT6 overexpressed BEAS-2B cells","study_abstract":"Comprehensive identification and characterization of the binding sites of STAT6 in STAT6 overexpressed BEAS-2B cells. We used ChIP-Seq method, in which next gene sequencing technology and chromatin-immunoprecipitation assay were combined.","study_primary_id":"DRP000043"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"DRP000178","sample_accession":"DRS000240","experiment_accession":"DRX000240","run_accession":"DRR000442","run_center_name":"UT-MGS","machine_type":"Illumina Genome Analyzer II","paired_end":false,"study_title":"Comprehensive identification and characterization of the binding sites of HIF-1alpha","study_abstract":"Comprehensive identification and characterization of the binding sites of HIF-1alpha in mammalian genes were attempted. We used ChIP-Seq method, in which next gene sequencing technology and chromatin-immunoprecipitation assay were combined.","study_primary_id":"DRP000178"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP013561","sample_accession":"ERS1015600","experiment_accession":"ERX1263643","run_accession":"ERR1190268","run_center_name":"ROSWELL PARK CANCER INSTITUTE","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Effect of hypoxia and atpenin A5 on the human monocyte transcriptome","study_abstract":"Monocyte-enriched peripheral blood mononuclear cells of apparently healthy human blood donors were cultured under normoxia or hypoxia (1% O2) for 24 hours at a high density (>20 million/ml). Normoxic cultures were also treated with 1 uM atpenin A5 for 48 hours. Afterwards, CD14+ monocytes were isolated using magnetic beads and their transcriptomes examined by sequencing rRNA-depleted total RNA (Illumina TruSeq Stranded Total RNA library preparation kit; HiSeq 2000 sequencer; paired 101 b reads; 6 libraries per flow lane).","study_primary_id":"ERP013561"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP013561","sample_accession":"ERS1015603","experiment_accession":"ERX1263646","run_accession":"ERR1190271","run_center_name":"ROSWELL PARK CANCER INSTITUTE","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Effect of hypoxia and atpenin A5 on the human monocyte transcriptome","study_abstract":"Monocyte-enriched peripheral blood mononuclear cells of apparently healthy human blood donors were cultured under normoxia or hypoxia (1% O2) for 24 hours at a high density (>20 million/ml). Normoxic cultures were also treated with 1 uM atpenin A5 for 48 hours. Afterwards, CD14+ monocytes were isolated using magnetic beads and their transcriptomes examined by sequencing rRNA-depleted total RNA (Illumina TruSeq Stranded Total RNA library preparation kit; HiSeq 2000 sequencer; paired 101 b reads; 6 libraries per flow lane).","study_primary_id":"ERP013561"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP013561","sample_accession":"ERS1015601","experiment_accession":"ERX1263644","run_accession":"ERR1190269","run_center_name":"ROSWELL PARK CANCER INSTITUTE","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Effect of hypoxia and atpenin A5 on the human monocyte transcriptome","study_abstract":"Monocyte-enriched peripheral blood mononuclear cells of apparently healthy human blood donors were cultured under normoxia or hypoxia (1% O2) for 24 hours at a high density (>20 million/ml). Normoxic cultures were also treated with 1 uM atpenin A5 for 48 hours. Afterwards, CD14+ monocytes were isolated using magnetic beads and their transcriptomes examined by sequencing rRNA-depleted total RNA (Illumina TruSeq Stranded Total RNA library preparation kit; HiSeq 2000 sequencer; paired 101 b reads; 6 libraries per flow lane).","study_primary_id":"ERP013561"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP013561","sample_accession":"ERS1015602","experiment_accession":"ERX1263645","run_accession":"ERR1190270","run_center_name":"ROSWELL PARK CANCER INSTITUTE","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Effect of hypoxia and atpenin A5 on the human monocyte transcriptome","study_abstract":"Monocyte-enriched peripheral blood mononuclear cells of apparently healthy human blood donors were cultured under normoxia or hypoxia (1% O2) for 24 hours at a high density (>20 million/ml). Normoxic cultures were also treated with 1 uM atpenin A5 for 48 hours. Afterwards, CD14+ monocytes were isolated using magnetic beads and their transcriptomes examined by sequencing rRNA-depleted total RNA (Illumina TruSeq Stranded Total RNA library preparation kit; HiSeq 2000 sequencer; paired 101 b reads; 6 libraries per flow lane).","study_primary_id":"ERP013561"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP013561","sample_accession":"ERS1015604","experiment_accession":"ERX1263647","run_accession":"ERR1190272","run_center_name":"ROSWELL PARK CANCER INSTITUTE","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Effect of hypoxia and atpenin A5 on the human monocyte transcriptome","study_abstract":"Monocyte-enriched peripheral blood mononuclear cells of apparently healthy human blood donors were cultured under normoxia or hypoxia (1% O2) for 24 hours at a high density (>20 million/ml). Normoxic cultures were also treated with 1 uM atpenin A5 for 48 hours. Afterwards, CD14+ monocytes were isolated using magnetic beads and their transcriptomes examined by sequencing rRNA-depleted total RNA (Illumina TruSeq Stranded Total RNA library preparation kit; HiSeq 2000 sequencer; paired 101 b reads; 6 libraries per flow lane).","study_primary_id":"ERP013561"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP013561","sample_accession":"ERS1015598","experiment_accession":"ERX1263641","run_accession":"ERR1190266","run_center_name":"ROSWELL PARK CANCER INSTITUTE","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Effect of hypoxia and atpenin A5 on the human monocyte transcriptome","study_abstract":"Monocyte-enriched peripheral blood mononuclear cells of apparently healthy human blood donors were cultured under normoxia or hypoxia (1% O2) for 24 hours at a high density (>20 million/ml). Normoxic cultures were also treated with 1 uM atpenin A5 for 48 hours. Afterwards, CD14+ monocytes were isolated using magnetic beads and their transcriptomes examined by sequencing rRNA-depleted total RNA (Illumina TruSeq Stranded Total RNA library preparation kit; HiSeq 2000 sequencer; paired 101 b reads; 6 libraries per flow lane).","study_primary_id":"ERP013561"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP013561","sample_accession":"ERS1015605","experiment_accession":"ERX1263648","run_accession":"ERR1190273","run_center_name":"ROSWELL PARK CANCER INSTITUTE","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Effect of hypoxia and atpenin A5 on the human monocyte transcriptome","study_abstract":"Monocyte-enriched peripheral blood mononuclear cells of apparently healthy human blood donors were cultured under normoxia or hypoxia (1% O2) for 24 hours at a high density (>20 million/ml). Normoxic cultures were also treated with 1 uM atpenin A5 for 48 hours. Afterwards, CD14+ monocytes were isolated using magnetic beads and their transcriptomes examined by sequencing rRNA-depleted total RNA (Illumina TruSeq Stranded Total RNA library preparation kit; HiSeq 2000 sequencer; paired 101 b reads; 6 libraries per flow lane).","study_primary_id":"ERP013561"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP013561","sample_accession":"ERS1015599","experiment_accession":"ERX1263642","run_accession":"ERR1190267","run_center_name":"ROSWELL PARK CANCER INSTITUTE","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Effect of hypoxia and atpenin A5 on the human monocyte transcriptome","study_abstract":"Monocyte-enriched peripheral blood mononuclear cells of apparently healthy human blood donors were cultured under normoxia or hypoxia (1% O2) for 24 hours at a high density (>20 million/ml). Normoxic cultures were also treated with 1 uM atpenin A5 for 48 hours. Afterwards, CD14+ monocytes were isolated using magnetic beads and their transcriptomes examined by sequencing rRNA-depleted total RNA (Illumina TruSeq Stranded Total RNA library preparation kit; HiSeq 2000 sequencer; paired 101 b reads; 6 libraries per flow lane).","study_primary_id":"ERP013561"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP013561","sample_accession":"ERS1015606","experiment_accession":"ERX1263649","run_accession":"ERR1190274","run_center_name":"ROSWELL PARK CANCER INSTITUTE","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Effect of hypoxia and atpenin A5 on the human monocyte transcriptome","study_abstract":"Monocyte-enriched peripheral blood mononuclear cells of apparently healthy human blood donors were cultured under normoxia or hypoxia (1% O2) for 24 hours at a high density (>20 million/ml). Normoxic cultures were also treated with 1 uM atpenin A5 for 48 hours. Afterwards, CD14+ monocytes were isolated using magnetic beads and their transcriptomes examined by sequencing rRNA-depleted total RNA (Illumina TruSeq Stranded Total RNA library preparation kit; HiSeq 2000 sequencer; paired 101 b reads; 6 libraries per flow lane).","study_primary_id":"ERP013561"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928691","experiment_accession":"ERX2180877","run_accession":"ERR2124025","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928691","experiment_accession":"ERX2180865","run_accession":"ERR2124013","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928691","experiment_accession":"ERX2180883","run_accession":"ERR2124031","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928691","experiment_accession":"ERX2180871","run_accession":"ERR2124019","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928691","experiment_accession":"ERX2180889","run_accession":"ERR2124037","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928691","experiment_accession":"ERX2180895","run_accession":"ERR2124043","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928689","experiment_accession":"ERX2180869","run_accession":"ERR2124017","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928689","experiment_accession":"ERX2180893","run_accession":"ERR2124041","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928689","experiment_accession":"ERX2180875","run_accession":"ERR2124023","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928689","experiment_accession":"ERX2180887","run_accession":"ERR2124035","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928689","experiment_accession":"ERX2180863","run_accession":"ERR2124011","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928689","experiment_accession":"ERX2180881","run_accession":"ERR2124029","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928686","experiment_accession":"ERX2180860","run_accession":"ERR2124008","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928686","experiment_accession":"ERX2180878","run_accession":"ERR2124026","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928686","experiment_accession":"ERX2180866","run_accession":"ERR2124014","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928686","experiment_accession":"ERX2180884","run_accession":"ERR2124032","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928686","experiment_accession":"ERX2180890","run_accession":"ERR2124038","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928686","experiment_accession":"ERX2180872","run_accession":"ERR2124020","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928687","experiment_accession":"ERX2180867","run_accession":"ERR2124015","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928687","experiment_accession":"ERX2180891","run_accession":"ERR2124039","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928687","experiment_accession":"ERX2180861","run_accession":"ERR2124009","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928687","experiment_accession":"ERX2180873","run_accession":"ERR2124021","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928687","experiment_accession":"ERX2180879","run_accession":"ERR2124027","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928687","experiment_accession":"ERX2180885","run_accession":"ERR2124033","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928690","experiment_accession":"ERX2180864","run_accession":"ERR2124012","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928690","experiment_accession":"ERX2180894","run_accession":"ERR2124042","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928690","experiment_accession":"ERX2180882","run_accession":"ERR2124030","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928690","experiment_accession":"ERX2180870","run_accession":"ERR2124018","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928690","experiment_accession":"ERX2180888","run_accession":"ERR2124036","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928690","experiment_accession":"ERX2180876","run_accession":"ERR2124024","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928688","experiment_accession":"ERX2180880","run_accession":"ERR2124028","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928688","experiment_accession":"ERX2180862","run_accession":"ERR2124010","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928688","experiment_accession":"ERX2180868","run_accession":"ERR2124016","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928688","experiment_accession":"ERX2180892","run_accession":"ERR2124040","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928688","experiment_accession":"ERX2180886","run_accession":"ERR2124034","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"ERP104309","sample_accession":"ERS1928688","experiment_accession":"ERX2180874","run_accession":"ERR2124022","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"SRPK1_is_a_therapeutic_vulnerability_in_acute_myeloid_leukemia_through_its_effects_on_isoform_choice_of_epigenetic_regulators__","study_abstract":"Acute myeloid leukemia (AML) is an aggressive cancer of hematopoietic stem cells that remains lethal for most sufferers. Having recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of AML, here we investigate the molecular basis and therapeutic potential of this finding. First, we show that genetic or pharmacological inhibition of SRPK1 induces cell cycle arrest, leukemic cell differentiation and prolongation of survival of immunocompromised mice transplanted with AML cells. We go on to show that SRPK1 inhibition led to altered isoform levels of many genes including several with roles in leukemogenesis such as MYB and MED24. Collectively our findings reveal that SRPK1 is required for normal splicing of key epigenetic regulators and forms a novel a therapeutic vulnerability in AML.","study_primary_id":"ERP104309"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP000405","sample_accession":"SRS001800","experiment_accession":"SRX001883","run_accession":"SRR006578","run_center_name":"UTGSFSCB-ML","machine_type":"Illumina Genome Analyzer","paired_end":false,"study_title":"De novo short read clustering study","study_abstract":"De novo short read clustering study","study_primary_id":"SRP000405"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP005697","sample_accession":"SRS172516","experiment_accession":"SRX042194","run_accession":"SRR100173","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer II","paired_end":false,"study_title":"GSE27221: ENCODE Genome Institute of Singapore RNA-Seq","study_abstract":".","study_primary_id":"SRP005697"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP005697","sample_accession":"SRS172517","experiment_accession":"SRX042195","run_accession":"SRR100174","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer II","paired_end":false,"study_title":"GSE27221: ENCODE Genome Institute of Singapore RNA-Seq","study_abstract":".","study_primary_id":"SRP005697"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP005697","sample_accession":"SRS172630","experiment_accession":"SRX042348","run_accession":"SRR100289","run_center_name":"GEO","machine_type":"AB SOLiD System 3.0","paired_end":false,"study_title":"GSE27221: ENCODE Genome Institute of Singapore RNA-Seq","study_abstract":".","study_primary_id":"SRP005697"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281395","experiment_accession":"SRX110054","run_accession":"SRR387434","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281408","experiment_accession":"SRX110067","run_accession":"SRR387447","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281406","experiment_accession":"SRX110065","run_accession":"SRR387445","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281392","experiment_accession":"SRX110052","run_accession":"SRR387432","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281385","experiment_accession":"SRX110045","run_accession":"SRR387418","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281386","experiment_accession":"SRX110046","run_accession":"SRR387426","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS270291","experiment_accession":"SRX105537","run_accession":"SRR387398","run_center_name":"CIT","machine_type":"Illumina Genome Analyzer IIx","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281387","experiment_accession":"SRX110047","run_accession":"SRR387427","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS270289","experiment_accession":"SRX105535","run_accession":"SRR387396","run_center_name":"CIT","machine_type":"Illumina Genome Analyzer IIx","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS270293","experiment_accession":"SRX105539","run_accession":"SRR387400","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS270288","experiment_accession":"SRX105534","run_accession":"SRR387395","run_center_name":"CIT","machine_type":"Illumina Genome Analyzer IIx","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281393","experiment_accession":"SRX110053","run_accession":"SRR387433","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281400","experiment_accession":"SRX110059","run_accession":"SRR387439","run_center_name":"CIT","machine_type":"Illumina Genome Analyzer IIx","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS270290","experiment_accession":"SRX105536","run_accession":"SRR387397","run_center_name":"CIT","machine_type":"Illumina Genome Analyzer IIx","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281402","experiment_accession":"SRX110061","run_accession":"SRR387441","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281384","experiment_accession":"SRX110044","run_accession":"SRR387407","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281404","experiment_accession":"SRX110063","run_accession":"SRR387443","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281409","experiment_accession":"SRX110068","run_accession":"SRR387448","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281407","experiment_accession":"SRX110066","run_accession":"SRR387446","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281403","experiment_accession":"SRX110062","run_accession":"SRR387442","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS270284","experiment_accession":"SRX105530","run_accession":"SRR387392","run_center_name":"CIT","machine_type":"Illumina Genome Analyzer IIx","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS270286","experiment_accession":"SRX105532","run_accession":"SRR387394","run_center_name":"CIT","machine_type":"Illumina Genome Analyzer IIx","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281382","experiment_accession":"SRX110042","run_accession":"SRR387405","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281401","experiment_accession":"SRX110060","run_accession":"SRR387440","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281390","experiment_accession":"SRX110050","run_accession":"SRR387430","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS270287","experiment_accession":"SRX105533","run_accession":"SRR387293","run_center_name":"CIT","machine_type":"Illumina Genome Analyzer IIx","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281388","experiment_accession":"SRX110048","run_accession":"SRR387428","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281399","experiment_accession":"SRX110058","run_accession":"SRR387438","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS270294","experiment_accession":"SRX105540","run_accession":"SRR387401","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281396","experiment_accession":"SRX110055","run_accession":"SRR387435","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281405","experiment_accession":"SRX110064","run_accession":"SRR387444","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281389","experiment_accession":"SRX110049","run_accession":"SRR387429","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281397","experiment_accession":"SRX110056","run_accession":"SRR387436","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281383","experiment_accession":"SRX110043","run_accession":"SRR387406","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS270296","experiment_accession":"SRX105542","run_accession":"SRR387403","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS270285","experiment_accession":"SRX105531","run_accession":"SRR387393","run_center_name":"CIT","machine_type":"Illumina Genome Analyzer IIx","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS270295","experiment_accession":"SRX105541","run_accession":"SRR387402","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281391","experiment_accession":"SRX110051","run_accession":"SRR387431","run_center_name":"CIT","machine_type":"Illumina Genome Analyzer IIx","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281381","experiment_accession":"SRX110041","run_accession":"SRR387404","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS270292","experiment_accession":"SRX105538","run_accession":"SRR387399","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP009316","sample_accession":"SRS281398","experiment_accession":"SRX110057","run_accession":"SRR387437","run_center_name":"CIT","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Burkitt Lymphoma Pathogenesis and Therapeutic Targets from Structural and Functional Genomics","study_abstract":"Burkitt lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. We used high throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways that cooperate with MYC, the defining oncogene of this cancer. In 38% of sporadic BL (sBL) cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. In 70% of sBL cases, mutations affecting the transcription factor TCF3 or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival PI(3) kinase pathway in BL, in part by augmenting constitutive B cell receptor signaling. These findings suggest opportunities to improve therapy for patients with BL.","study_primary_id":"SRP009316"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP017294","sample_accession":"SRS376877","experiment_accession":"SRX206191","run_accession":"SRR619803","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer II","paired_end":false,"study_title":"Genomewide analysis of U1C-dependent alternative splicing","study_abstract":"To investigate whether U1C plays a role in splicing regulation in human system, we performed siRNA-mediated knockdown of U1C in HeLa cells and analyzed alternative splicing patterns by high-throughput RNA sequencing (RNAseq) Overall design: RNAseq performed with poly(A)+ selected total RNA from U1C-knockdown and control-treated HeLa cells","study_primary_id":"SRP017294"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP017294","sample_accession":"SRS376877","experiment_accession":"SRX206191","run_accession":"SRR619804","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer II","paired_end":false,"study_title":"Genomewide analysis of U1C-dependent alternative splicing","study_abstract":"To investigate whether U1C plays a role in splicing regulation in human system, we performed siRNA-mediated knockdown of U1C in HeLa cells and analyzed alternative splicing patterns by high-throughput RNA sequencing (RNAseq) Overall design: RNAseq performed with poly(A)+ selected total RNA from U1C-knockdown and control-treated HeLa cells","study_primary_id":"SRP017294"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP017294","sample_accession":"SRS376878","experiment_accession":"SRX206192","run_accession":"SRR619805","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer II","paired_end":false,"study_title":"Genomewide analysis of U1C-dependent alternative splicing","study_abstract":"To investigate whether U1C plays a role in splicing regulation in human system, we performed siRNA-mediated knockdown of U1C in HeLa cells and analyzed alternative splicing patterns by high-throughput RNA sequencing (RNAseq) Overall design: RNAseq performed with poly(A)+ selected total RNA from U1C-knockdown and control-treated HeLa cells","study_primary_id":"SRP017294"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP017294","sample_accession":"SRS376878","experiment_accession":"SRX206192","run_accession":"SRR619806","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer II","paired_end":false,"study_title":"Genomewide analysis of U1C-dependent alternative splicing","study_abstract":"To investigate whether U1C plays a role in splicing regulation in human system, we performed siRNA-mediated knockdown of U1C in HeLa cells and analyzed alternative splicing patterns by high-throughput RNA sequencing (RNAseq) Overall design: RNAseq performed with poly(A)+ selected total RNA from U1C-knockdown and control-treated HeLa cells","study_primary_id":"SRP017294"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018304","sample_accession":"SRS388260","experiment_accession":"SRX220702","run_accession":"SRR653897","run_center_name":"Trinity College Dublin","machine_type":"Illumina Genome Analyzer II","paired_end":false,"study_title":"Homo sapiens Transcriptome or Gene expression","study_abstract":"Access RNA-seq data as a source of SNP calls.","study_primary_id":"SRP018304"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396267","experiment_accession":"SRX241561","run_accession":"SRR741887","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396272","experiment_accession":"SRX241566","run_accession":"SRR741892","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396286","experiment_accession":"SRX241580","run_accession":"SRR741906","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396269","experiment_accession":"SRX241563","run_accession":"SRR741889","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396273","experiment_accession":"SRX241567","run_accession":"SRR741893","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396277","experiment_accession":"SRX241571","run_accession":"SRR741897","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396285","experiment_accession":"SRX241579","run_accession":"SRR741905","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396264","experiment_accession":"SRX241558","run_accession":"SRR741884","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396265","experiment_accession":"SRX241559","run_accession":"SRR741885","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396271","experiment_accession":"SRX241565","run_accession":"SRR741891","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396284","experiment_accession":"SRX241578","run_accession":"SRR741904","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396266","experiment_accession":"SRX241560","run_accession":"SRR741886","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396268","experiment_accession":"SRX241562","run_accession":"SRR741888","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396276","experiment_accession":"SRX241570","run_accession":"SRR741896","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396279","experiment_accession":"SRX241573","run_accession":"SRR741899","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396283","experiment_accession":"SRX241577","run_accession":"SRR741903","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396280","experiment_accession":"SRX241574","run_accession":"SRR741900","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396278","experiment_accession":"SRX241572","run_accession":"SRR741898","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396282","experiment_accession":"SRX241576","run_accession":"SRR741902","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396287","experiment_accession":"SRX241581","run_accession":"SRR741907","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396274","experiment_accession":"SRX241568","run_accession":"SRR741894","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396270","experiment_accession":"SRX241564","run_accession":"SRR741890","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396281","experiment_accession":"SRX241575","run_accession":"SRR741901","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP018716","sample_accession":"SRS396275","experiment_accession":"SRX241569","run_accession":"SRR741895","run_center_name":"GEO","machine_type":"Illumina Genome Analyzer IIx","paired_end":false,"study_title":"Remodeling of Ago2-mRNA interactions upon cellular stress reflects miRNA complementarity and correlates with altered translation rates (part 1)","study_abstract":"When adapting to environmental stress, cells attenuate and reprogram their translational output. In part, these altered translation profiles are established through changes in the interactions between RNA-binding proteins and mRNAs. The Ago2/microRNA machinery has been shown to participate in stress-induced translational upregulation of a particular mRNA, CAT-1; however, a detailed, transcriptome-wide understanding of the involvement of Ago2 in the process has been lacking. Here, we profiled the overall changes in Ago2-mRNA interactions upon arsenite stress by CLIP-seq. Ago2 displayed a significant remodeling of its transcript occupancy, with the majority of 3` UTR and CDS sites exhibiting stronger interaction. Interestingly, target sites that were destined for release from Ago2 upon stress were depleted in miRNA complementarity signatures, suggesting an alternative mode of interaction. To compare the changes in Ago2 binding patterns across transcripts with changes in their translational states, we measured mRNA profiles on ribosome/polysome gradients by RNA-seq. Increased Ago2 occupancy correlated with stronger repression of translation for those mRNAs, as evidenced by a shift toward lighter gradient fractions upon stress, while release of Ago2 was associated with the limited number of transcripts that remained translated. Taken together, these data point to a role for Ago2 and the mammalian microRNAs in mediating the translational component of the stress response. Overall design: In this sub-series, CLIP and RNAseq data from the arsenite treatment experiment are presented. Experiments on 293S cells +/- arsenite treatment, in 4 biological replicates. On each treatment/replicate biological sample, both a CLIP-seq protocol and an RNA-seq protocol were performed, so these datasets are “paired” in addition to the treatment pairing.","study_primary_id":"SRP018716"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP029990","sample_accession":"SRS481300","experiment_accession":"SRX352333","run_accession":"SRR988501","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Molecular Hallmarks of Experimentally Acquired Immunity to Malaria [Pilot Study]","study_abstract":"Sterile immunity to Plasmodium falciparum infection can be induced experimentally in humans after few exposures. An example is the induction of immunity using whole parasites by exposure of malaria-naive volunteers to infectious mosquito bites while using chloroquine prophylaxis (CPS immunization). Chloroquine kills blood-stage parasites but leaves liver-stage parasites unaffected, thereby exposing the liver-stage and early blood-stage antigens to the immune system. Upon subsequent challenge, volunteers are completely protected from infection, but protective efficacy decreases when fewer infectious mosquito bites are used for CPS immunization. Efforts to understand the mechanisms of this immunity, and how it differs from naturally-acquired immunity, may provide critical insights that could aid malaria vaccine development. In this pilot study, transcriptomic features are derived from blood samples collected before and after challenge with infectious mosquito bites. Overall design: 12 samples; paired pre- and post-challenge for 5 individuals, plus two controls","study_primary_id":"SRP029990"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP029990","sample_accession":"SRS481307","experiment_accession":"SRX352340","run_accession":"SRR988508","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Molecular Hallmarks of Experimentally Acquired Immunity to Malaria [Pilot Study]","study_abstract":"Sterile immunity to Plasmodium falciparum infection can be induced experimentally in humans after few exposures. An example is the induction of immunity using whole parasites by exposure of malaria-naive volunteers to infectious mosquito bites while using chloroquine prophylaxis (CPS immunization). Chloroquine kills blood-stage parasites but leaves liver-stage parasites unaffected, thereby exposing the liver-stage and early blood-stage antigens to the immune system. Upon subsequent challenge, volunteers are completely protected from infection, but protective efficacy decreases when fewer infectious mosquito bites are used for CPS immunization. Efforts to understand the mechanisms of this immunity, and how it differs from naturally-acquired immunity, may provide critical insights that could aid malaria vaccine development. In this pilot study, transcriptomic features are derived from blood samples collected before and after challenge with infectious mosquito bites. Overall design: 12 samples; paired pre- and post-challenge for 5 individuals, plus two controls","study_primary_id":"SRP029990"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP029990","sample_accession":"SRS481308","experiment_accession":"SRX352341","run_accession":"SRR988509","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Molecular Hallmarks of Experimentally Acquired Immunity to Malaria [Pilot Study]","study_abstract":"Sterile immunity to Plasmodium falciparum infection can be induced experimentally in humans after few exposures. An example is the induction of immunity using whole parasites by exposure of malaria-naive volunteers to infectious mosquito bites while using chloroquine prophylaxis (CPS immunization). Chloroquine kills blood-stage parasites but leaves liver-stage parasites unaffected, thereby exposing the liver-stage and early blood-stage antigens to the immune system. Upon subsequent challenge, volunteers are completely protected from infection, but protective efficacy decreases when fewer infectious mosquito bites are used for CPS immunization. Efforts to understand the mechanisms of this immunity, and how it differs from naturally-acquired immunity, may provide critical insights that could aid malaria vaccine development. In this pilot study, transcriptomic features are derived from blood samples collected before and after challenge with infectious mosquito bites. Overall design: 12 samples; paired pre- and post-challenge for 5 individuals, plus two controls","study_primary_id":"SRP029990"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP029990","sample_accession":"SRS481304","experiment_accession":"SRX352337","run_accession":"SRR988505","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Molecular Hallmarks of Experimentally Acquired Immunity to Malaria [Pilot Study]","study_abstract":"Sterile immunity to Plasmodium falciparum infection can be induced experimentally in humans after few exposures. An example is the induction of immunity using whole parasites by exposure of malaria-naive volunteers to infectious mosquito bites while using chloroquine prophylaxis (CPS immunization). Chloroquine kills blood-stage parasites but leaves liver-stage parasites unaffected, thereby exposing the liver-stage and early blood-stage antigens to the immune system. Upon subsequent challenge, volunteers are completely protected from infection, but protective efficacy decreases when fewer infectious mosquito bites are used for CPS immunization. Efforts to understand the mechanisms of this immunity, and how it differs from naturally-acquired immunity, may provide critical insights that could aid malaria vaccine development. In this pilot study, transcriptomic features are derived from blood samples collected before and after challenge with infectious mosquito bites. Overall design: 12 samples; paired pre- and post-challenge for 5 individuals, plus two controls","study_primary_id":"SRP029990"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP029990","sample_accession":"SRS481299","experiment_accession":"SRX352332","run_accession":"SRR988500","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Molecular Hallmarks of Experimentally Acquired Immunity to Malaria [Pilot Study]","study_abstract":"Sterile immunity to Plasmodium falciparum infection can be induced experimentally in humans after few exposures. An example is the induction of immunity using whole parasites by exposure of malaria-naive volunteers to infectious mosquito bites while using chloroquine prophylaxis (CPS immunization). Chloroquine kills blood-stage parasites but leaves liver-stage parasites unaffected, thereby exposing the liver-stage and early blood-stage antigens to the immune system. Upon subsequent challenge, volunteers are completely protected from infection, but protective efficacy decreases when fewer infectious mosquito bites are used for CPS immunization. Efforts to understand the mechanisms of this immunity, and how it differs from naturally-acquired immunity, may provide critical insights that could aid malaria vaccine development. In this pilot study, transcriptomic features are derived from blood samples collected before and after challenge with infectious mosquito bites. Overall design: 12 samples; paired pre- and post-challenge for 5 individuals, plus two controls","study_primary_id":"SRP029990"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP029990","sample_accession":"SRS481306","experiment_accession":"SRX352339","run_accession":"SRR988507","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Molecular Hallmarks of Experimentally Acquired Immunity to Malaria [Pilot Study]","study_abstract":"Sterile immunity to Plasmodium falciparum infection can be induced experimentally in humans after few exposures. An example is the induction of immunity using whole parasites by exposure of malaria-naive volunteers to infectious mosquito bites while using chloroquine prophylaxis (CPS immunization). Chloroquine kills blood-stage parasites but leaves liver-stage parasites unaffected, thereby exposing the liver-stage and early blood-stage antigens to the immune system. Upon subsequent challenge, volunteers are completely protected from infection, but protective efficacy decreases when fewer infectious mosquito bites are used for CPS immunization. Efforts to understand the mechanisms of this immunity, and how it differs from naturally-acquired immunity, may provide critical insights that could aid malaria vaccine development. In this pilot study, transcriptomic features are derived from blood samples collected before and after challenge with infectious mosquito bites. Overall design: 12 samples; paired pre- and post-challenge for 5 individuals, plus two controls","study_primary_id":"SRP029990"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP029990","sample_accession":"SRS481302","experiment_accession":"SRX352335","run_accession":"SRR988503","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Molecular Hallmarks of Experimentally Acquired Immunity to Malaria [Pilot Study]","study_abstract":"Sterile immunity to Plasmodium falciparum infection can be induced experimentally in humans after few exposures. An example is the induction of immunity using whole parasites by exposure of malaria-naive volunteers to infectious mosquito bites while using chloroquine prophylaxis (CPS immunization). Chloroquine kills blood-stage parasites but leaves liver-stage parasites unaffected, thereby exposing the liver-stage and early blood-stage antigens to the immune system. Upon subsequent challenge, volunteers are completely protected from infection, but protective efficacy decreases when fewer infectious mosquito bites are used for CPS immunization. Efforts to understand the mechanisms of this immunity, and how it differs from naturally-acquired immunity, may provide critical insights that could aid malaria vaccine development. In this pilot study, transcriptomic features are derived from blood samples collected before and after challenge with infectious mosquito bites. Overall design: 12 samples; paired pre- and post-challenge for 5 individuals, plus two controls","study_primary_id":"SRP029990"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP029990","sample_accession":"SRS481305","experiment_accession":"SRX352338","run_accession":"SRR988506","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Molecular Hallmarks of Experimentally Acquired Immunity to Malaria [Pilot Study]","study_abstract":"Sterile immunity to Plasmodium falciparum infection can be induced experimentally in humans after few exposures. An example is the induction of immunity using whole parasites by exposure of malaria-naive volunteers to infectious mosquito bites while using chloroquine prophylaxis (CPS immunization). Chloroquine kills blood-stage parasites but leaves liver-stage parasites unaffected, thereby exposing the liver-stage and early blood-stage antigens to the immune system. Upon subsequent challenge, volunteers are completely protected from infection, but protective efficacy decreases when fewer infectious mosquito bites are used for CPS immunization. Efforts to understand the mechanisms of this immunity, and how it differs from naturally-acquired immunity, may provide critical insights that could aid malaria vaccine development. In this pilot study, transcriptomic features are derived from blood samples collected before and after challenge with infectious mosquito bites. Overall design: 12 samples; paired pre- and post-challenge for 5 individuals, plus two controls","study_primary_id":"SRP029990"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP029990","sample_accession":"SRS481303","experiment_accession":"SRX352336","run_accession":"SRR988504","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Molecular Hallmarks of Experimentally Acquired Immunity to Malaria [Pilot Study]","study_abstract":"Sterile immunity to Plasmodium falciparum infection can be induced experimentally in humans after few exposures. An example is the induction of immunity using whole parasites by exposure of malaria-naive volunteers to infectious mosquito bites while using chloroquine prophylaxis (CPS immunization). Chloroquine kills blood-stage parasites but leaves liver-stage parasites unaffected, thereby exposing the liver-stage and early blood-stage antigens to the immune system. Upon subsequent challenge, volunteers are completely protected from infection, but protective efficacy decreases when fewer infectious mosquito bites are used for CPS immunization. Efforts to understand the mechanisms of this immunity, and how it differs from naturally-acquired immunity, may provide critical insights that could aid malaria vaccine development. In this pilot study, transcriptomic features are derived from blood samples collected before and after challenge with infectious mosquito bites. Overall design: 12 samples; paired pre- and post-challenge for 5 individuals, plus two controls","study_primary_id":"SRP029990"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP029990","sample_accession":"SRS481301","experiment_accession":"SRX352334","run_accession":"SRR988502","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Molecular Hallmarks of Experimentally Acquired Immunity to Malaria [Pilot Study]","study_abstract":"Sterile immunity to Plasmodium falciparum infection can be induced experimentally in humans after few exposures. An example is the induction of immunity using whole parasites by exposure of malaria-naive volunteers to infectious mosquito bites while using chloroquine prophylaxis (CPS immunization). Chloroquine kills blood-stage parasites but leaves liver-stage parasites unaffected, thereby exposing the liver-stage and early blood-stage antigens to the immune system. Upon subsequent challenge, volunteers are completely protected from infection, but protective efficacy decreases when fewer infectious mosquito bites are used for CPS immunization. Efforts to understand the mechanisms of this immunity, and how it differs from naturally-acquired immunity, may provide critical insights that could aid malaria vaccine development. In this pilot study, transcriptomic features are derived from blood samples collected before and after challenge with infectious mosquito bites. Overall design: 12 samples; paired pre- and post-challenge for 5 individuals, plus two controls","study_primary_id":"SRP029990"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP029990","sample_accession":"SRS481309","experiment_accession":"SRX352342","run_accession":"SRR988510","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Molecular Hallmarks of Experimentally Acquired Immunity to Malaria [Pilot Study]","study_abstract":"Sterile immunity to Plasmodium falciparum infection can be induced experimentally in humans after few exposures. An example is the induction of immunity using whole parasites by exposure of malaria-naive volunteers to infectious mosquito bites while using chloroquine prophylaxis (CPS immunization). Chloroquine kills blood-stage parasites but leaves liver-stage parasites unaffected, thereby exposing the liver-stage and early blood-stage antigens to the immune system. Upon subsequent challenge, volunteers are completely protected from infection, but protective efficacy decreases when fewer infectious mosquito bites are used for CPS immunization. Efforts to understand the mechanisms of this immunity, and how it differs from naturally-acquired immunity, may provide critical insights that could aid malaria vaccine development. In this pilot study, transcriptomic features are derived from blood samples collected before and after challenge with infectious mosquito bites. Overall design: 12 samples; paired pre- and post-challenge for 5 individuals, plus two controls","study_primary_id":"SRP029990"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP029990","sample_accession":"SRS481298","experiment_accession":"SRX352331","run_accession":"SRR988499","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Molecular Hallmarks of Experimentally Acquired Immunity to Malaria [Pilot Study]","study_abstract":"Sterile immunity to Plasmodium falciparum infection can be induced experimentally in humans after few exposures. An example is the induction of immunity using whole parasites by exposure of malaria-naive volunteers to infectious mosquito bites while using chloroquine prophylaxis (CPS immunization). Chloroquine kills blood-stage parasites but leaves liver-stage parasites unaffected, thereby exposing the liver-stage and early blood-stage antigens to the immune system. Upon subsequent challenge, volunteers are completely protected from infection, but protective efficacy decreases when fewer infectious mosquito bites are used for CPS immunization. Efforts to understand the mechanisms of this immunity, and how it differs from naturally-acquired immunity, may provide critical insights that could aid malaria vaccine development. In this pilot study, transcriptomic features are derived from blood samples collected before and after challenge with infectious mosquito bites. Overall design: 12 samples; paired pre- and post-challenge for 5 individuals, plus two controls","study_primary_id":"SRP029990"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP033116","sample_accession":"SRS503486","experiment_accession":"SRX378921","run_accession":"SRR1032139","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":false,"study_title":"Ribonuclease L and Metal-Ion-Independent Endoribonuclease Cleavage Sites in Host and Viral RNAs","study_abstract":"We used 2', 3'-cyclic phosphate cDNA synthesis and Illumina sequencing to identify and quantify metal-ion-independent endoribonuclease cleavage sites in host and viral RNAs. Overall design: To make cDNA libraries, we exploited the 2’, 3’-cyclic phosphate at the end of RNA fragments produced by RNase L and other metal-ion-independent endoribonucleases. Using Arabidopsis thaliana tRNA ligase, RNA fragments with 2’, 3’-cyclic phosphates were covalently attached to defined RNA linkers containing an 8-base long unique molecular identifier (UMI) sequence. Libraries prepared in this manner contain cDNA derived exclusively from RNA fragments with 2', 3'-cyclic phosphates. The UMI sequence allows for detailed quantitation. We optimized and validated 2’, 3’-cyclic phosphate cDNA synthesis and Illumina sequencing methods using viral RNAs cleaved with purified RNase L, viral RNAs cleaved with purified RNase A, and RNA from uninfected and poliovirus-infected HeLa cells.","study_primary_id":"SRP033116"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP033116","sample_accession":"SRS503482","experiment_accession":"SRX378917","run_accession":"SRR1032135","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":false,"study_title":"Ribonuclease L and Metal-Ion-Independent Endoribonuclease Cleavage Sites in Host and Viral RNAs","study_abstract":"We used 2', 3'-cyclic phosphate cDNA synthesis and Illumina sequencing to identify and quantify metal-ion-independent endoribonuclease cleavage sites in host and viral RNAs. Overall design: To make cDNA libraries, we exploited the 2’, 3’-cyclic phosphate at the end of RNA fragments produced by RNase L and other metal-ion-independent endoribonucleases. Using Arabidopsis thaliana tRNA ligase, RNA fragments with 2’, 3’-cyclic phosphates were covalently attached to defined RNA linkers containing an 8-base long unique molecular identifier (UMI) sequence. Libraries prepared in this manner contain cDNA derived exclusively from RNA fragments with 2', 3'-cyclic phosphates. The UMI sequence allows for detailed quantitation. We optimized and validated 2’, 3’-cyclic phosphate cDNA synthesis and Illumina sequencing methods using viral RNAs cleaved with purified RNase L, viral RNAs cleaved with purified RNase A, and RNA from uninfected and poliovirus-infected HeLa cells.","study_primary_id":"SRP033116"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP033116","sample_accession":"SRS503484","experiment_accession":"SRX378919","run_accession":"SRR1032137","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":false,"study_title":"Ribonuclease L and Metal-Ion-Independent Endoribonuclease Cleavage Sites in Host and Viral RNAs","study_abstract":"We used 2', 3'-cyclic phosphate cDNA synthesis and Illumina sequencing to identify and quantify metal-ion-independent endoribonuclease cleavage sites in host and viral RNAs. Overall design: To make cDNA libraries, we exploited the 2’, 3’-cyclic phosphate at the end of RNA fragments produced by RNase L and other metal-ion-independent endoribonucleases. Using Arabidopsis thaliana tRNA ligase, RNA fragments with 2’, 3’-cyclic phosphates were covalently attached to defined RNA linkers containing an 8-base long unique molecular identifier (UMI) sequence. Libraries prepared in this manner contain cDNA derived exclusively from RNA fragments with 2', 3'-cyclic phosphates. The UMI sequence allows for detailed quantitation. We optimized and validated 2’, 3’-cyclic phosphate cDNA synthesis and Illumina sequencing methods using viral RNAs cleaved with purified RNase L, viral RNAs cleaved with purified RNase A, and RNA from uninfected and poliovirus-infected HeLa cells.","study_primary_id":"SRP033116"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP033116","sample_accession":"SRS503477","experiment_accession":"SRX378912","run_accession":"SRR1032130","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":false,"study_title":"Ribonuclease L and Metal-Ion-Independent Endoribonuclease Cleavage Sites in Host and Viral RNAs","study_abstract":"We used 2', 3'-cyclic phosphate cDNA synthesis and Illumina sequencing to identify and quantify metal-ion-independent endoribonuclease cleavage sites in host and viral RNAs. Overall design: To make cDNA libraries, we exploited the 2’, 3’-cyclic phosphate at the end of RNA fragments produced by RNase L and other metal-ion-independent endoribonucleases. Using Arabidopsis thaliana tRNA ligase, RNA fragments with 2’, 3’-cyclic phosphates were covalently attached to defined RNA linkers containing an 8-base long unique molecular identifier (UMI) sequence. Libraries prepared in this manner contain cDNA derived exclusively from RNA fragments with 2', 3'-cyclic phosphates. The UMI sequence allows for detailed quantitation. We optimized and validated 2’, 3’-cyclic phosphate cDNA synthesis and Illumina sequencing methods using viral RNAs cleaved with purified RNase L, viral RNAs cleaved with purified RNase A, and RNA from uninfected and poliovirus-infected HeLa cells.","study_primary_id":"SRP033116"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP033116","sample_accession":"SRS503485","experiment_accession":"SRX378920","run_accession":"SRR1032138","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":false,"study_title":"Ribonuclease L and Metal-Ion-Independent Endoribonuclease Cleavage Sites in Host and Viral RNAs","study_abstract":"We used 2', 3'-cyclic phosphate cDNA synthesis and Illumina sequencing to identify and quantify metal-ion-independent endoribonuclease cleavage sites in host and viral RNAs. Overall design: To make cDNA libraries, we exploited the 2’, 3’-cyclic phosphate at the end of RNA fragments produced by RNase L and other metal-ion-independent endoribonucleases. Using Arabidopsis thaliana tRNA ligase, RNA fragments with 2’, 3’-cyclic phosphates were covalently attached to defined RNA linkers containing an 8-base long unique molecular identifier (UMI) sequence. Libraries prepared in this manner contain cDNA derived exclusively from RNA fragments with 2', 3'-cyclic phosphates. The UMI sequence allows for detailed quantitation. We optimized and validated 2’, 3’-cyclic phosphate cDNA synthesis and Illumina sequencing methods using viral RNAs cleaved with purified RNase L, viral RNAs cleaved with purified RNase A, and RNA from uninfected and poliovirus-infected HeLa cells.","study_primary_id":"SRP033116"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP033116","sample_accession":"SRS503483","experiment_accession":"SRX378918","run_accession":"SRR1032136","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":false,"study_title":"Ribonuclease L and Metal-Ion-Independent Endoribonuclease Cleavage Sites in Host and Viral RNAs","study_abstract":"We used 2', 3'-cyclic phosphate cDNA synthesis and Illumina sequencing to identify and quantify metal-ion-independent endoribonuclease cleavage sites in host and viral RNAs. Overall design: To make cDNA libraries, we exploited the 2’, 3’-cyclic phosphate at the end of RNA fragments produced by RNase L and other metal-ion-independent endoribonucleases. Using Arabidopsis thaliana tRNA ligase, RNA fragments with 2’, 3’-cyclic phosphates were covalently attached to defined RNA linkers containing an 8-base long unique molecular identifier (UMI) sequence. Libraries prepared in this manner contain cDNA derived exclusively from RNA fragments with 2', 3'-cyclic phosphates. The UMI sequence allows for detailed quantitation. We optimized and validated 2’, 3’-cyclic phosphate cDNA synthesis and Illumina sequencing methods using viral RNAs cleaved with purified RNase L, viral RNAs cleaved with purified RNase A, and RNA from uninfected and poliovirus-infected HeLa cells.","study_primary_id":"SRP033116"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP033116","sample_accession":"SRS503489","experiment_accession":"SRX378924","run_accession":"SRR1032142","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":false,"study_title":"Ribonuclease L and Metal-Ion-Independent Endoribonuclease Cleavage Sites in Host and Viral RNAs","study_abstract":"We used 2', 3'-cyclic phosphate cDNA synthesis and Illumina sequencing to identify and quantify metal-ion-independent endoribonuclease cleavage sites in host and viral RNAs. Overall design: To make cDNA libraries, we exploited the 2’, 3’-cyclic phosphate at the end of RNA fragments produced by RNase L and other metal-ion-independent endoribonucleases. Using Arabidopsis thaliana tRNA ligase, RNA fragments with 2’, 3’-cyclic phosphates were covalently attached to defined RNA linkers containing an 8-base long unique molecular identifier (UMI) sequence. Libraries prepared in this manner contain cDNA derived exclusively from RNA fragments with 2', 3'-cyclic phosphates. The UMI sequence allows for detailed quantitation. We optimized and validated 2’, 3’-cyclic phosphate cDNA synthesis and Illumina sequencing methods using viral RNAs cleaved with purified RNase L, viral RNAs cleaved with purified RNase A, and RNA from uninfected and poliovirus-infected HeLa cells.","study_primary_id":"SRP033116"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP033116","sample_accession":"SRS503490","experiment_accession":"SRX378925","run_accession":"SRR1032143","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":false,"study_title":"Ribonuclease L and Metal-Ion-Independent Endoribonuclease Cleavage Sites in Host and Viral RNAs","study_abstract":"We used 2', 3'-cyclic phosphate cDNA synthesis and Illumina sequencing to identify and quantify metal-ion-independent endoribonuclease cleavage sites in host and viral RNAs. Overall design: To make cDNA libraries, we exploited the 2’, 3’-cyclic phosphate at the end of RNA fragments produced by RNase L and other metal-ion-independent endoribonucleases. Using Arabidopsis thaliana tRNA ligase, RNA fragments with 2’, 3’-cyclic phosphates were covalently attached to defined RNA linkers containing an 8-base long unique molecular identifier (UMI) sequence. Libraries prepared in this manner contain cDNA derived exclusively from RNA fragments with 2', 3'-cyclic phosphates. The UMI sequence allows for detailed quantitation. We optimized and validated 2’, 3’-cyclic phosphate cDNA synthesis and Illumina sequencing methods using viral RNAs cleaved with purified RNase L, viral RNAs cleaved with purified RNase A, and RNA from uninfected and poliovirus-infected HeLa cells.","study_primary_id":"SRP033116"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP033116","sample_accession":"SRS503478","experiment_accession":"SRX378913","run_accession":"SRR1032131","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":false,"study_title":"Ribonuclease L and Metal-Ion-Independent Endoribonuclease Cleavage Sites in Host and Viral RNAs","study_abstract":"We used 2', 3'-cyclic phosphate cDNA synthesis and Illumina sequencing to identify and quantify metal-ion-independent endoribonuclease cleavage sites in host and viral RNAs. Overall design: To make cDNA libraries, we exploited the 2’, 3’-cyclic phosphate at the end of RNA fragments produced by RNase L and other metal-ion-independent endoribonucleases. Using Arabidopsis thaliana tRNA ligase, RNA fragments with 2’, 3’-cyclic phosphates were covalently attached to defined RNA linkers containing an 8-base long unique molecular identifier (UMI) sequence. Libraries prepared in this manner contain cDNA derived exclusively from RNA fragments with 2', 3'-cyclic phosphates. The UMI sequence allows for detailed quantitation. We optimized and validated 2’, 3’-cyclic phosphate cDNA synthesis and Illumina sequencing methods using viral RNAs cleaved with purified RNase L, viral RNAs cleaved with purified RNase A, and RNA from uninfected and poliovirus-infected HeLa cells.","study_primary_id":"SRP033116"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP033116","sample_accession":"SRS503488","experiment_accession":"SRX378923","run_accession":"SRR1032141","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":false,"study_title":"Ribonuclease L and Metal-Ion-Independent Endoribonuclease Cleavage Sites in Host and Viral RNAs","study_abstract":"We used 2', 3'-cyclic phosphate cDNA synthesis and Illumina sequencing to identify and quantify metal-ion-independent endoribonuclease cleavage sites in host and viral RNAs. Overall design: To make cDNA libraries, we exploited the 2’, 3’-cyclic phosphate at the end of RNA fragments produced by RNase L and other metal-ion-independent endoribonucleases. Using Arabidopsis thaliana tRNA ligase, RNA fragments with 2’, 3’-cyclic phosphates were covalently attached to defined RNA linkers containing an 8-base long unique molecular identifier (UMI) sequence. Libraries prepared in this manner contain cDNA derived exclusively from RNA fragments with 2', 3'-cyclic phosphates. The UMI sequence allows for detailed quantitation. We optimized and validated 2’, 3’-cyclic phosphate cDNA synthesis and Illumina sequencing methods using viral RNAs cleaved with purified RNase L, viral RNAs cleaved with purified RNase A, and RNA from uninfected and poliovirus-infected HeLa cells.","study_primary_id":"SRP033116"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP033116","sample_accession":"SRS503480","experiment_accession":"SRX378916","run_accession":"SRR1032134","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":false,"study_title":"Ribonuclease L and Metal-Ion-Independent Endoribonuclease Cleavage Sites in Host and Viral RNAs","study_abstract":"We used 2', 3'-cyclic phosphate cDNA synthesis and Illumina sequencing to identify and quantify metal-ion-independent endoribonuclease cleavage sites in host and viral RNAs. Overall design: To make cDNA libraries, we exploited the 2’, 3’-cyclic phosphate at the end of RNA fragments produced by RNase L and other metal-ion-independent endoribonucleases. Using Arabidopsis thaliana tRNA ligase, RNA fragments with 2’, 3’-cyclic phosphates were covalently attached to defined RNA linkers containing an 8-base long unique molecular identifier (UMI) sequence. Libraries prepared in this manner contain cDNA derived exclusively from RNA fragments with 2', 3'-cyclic phosphates. The UMI sequence allows for detailed quantitation. We optimized and validated 2’, 3’-cyclic phosphate cDNA synthesis and Illumina sequencing methods using viral RNAs cleaved with purified RNase L, viral RNAs cleaved with purified RNase A, and RNA from uninfected and poliovirus-infected HeLa cells.","study_primary_id":"SRP033116"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP033116","sample_accession":"SRS503487","experiment_accession":"SRX378922","run_accession":"SRR1032140","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":false,"study_title":"Ribonuclease L and Metal-Ion-Independent Endoribonuclease Cleavage Sites in Host and Viral RNAs","study_abstract":"We used 2', 3'-cyclic phosphate cDNA synthesis and Illumina sequencing to identify and quantify metal-ion-independent endoribonuclease cleavage sites in host and viral RNAs. Overall design: To make cDNA libraries, we exploited the 2’, 3’-cyclic phosphate at the end of RNA fragments produced by RNase L and other metal-ion-independent endoribonucleases. Using Arabidopsis thaliana tRNA ligase, RNA fragments with 2’, 3’-cyclic phosphates were covalently attached to defined RNA linkers containing an 8-base long unique molecular identifier (UMI) sequence. Libraries prepared in this manner contain cDNA derived exclusively from RNA fragments with 2', 3'-cyclic phosphates. The UMI sequence allows for detailed quantitation. We optimized and validated 2’, 3’-cyclic phosphate cDNA synthesis and Illumina sequencing methods using viral RNAs cleaved with purified RNase L, viral RNAs cleaved with purified RNase A, and RNA from uninfected and poliovirus-infected HeLa cells.","study_primary_id":"SRP033116"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP033116","sample_accession":"SRS503479","experiment_accession":"SRX378914","run_accession":"SRR1032132","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":false,"study_title":"Ribonuclease L and Metal-Ion-Independent Endoribonuclease Cleavage Sites in Host and Viral RNAs","study_abstract":"We used 2', 3'-cyclic phosphate cDNA synthesis and Illumina sequencing to identify and quantify metal-ion-independent endoribonuclease cleavage sites in host and viral RNAs. Overall design: To make cDNA libraries, we exploited the 2’, 3’-cyclic phosphate at the end of RNA fragments produced by RNase L and other metal-ion-independent endoribonucleases. Using Arabidopsis thaliana tRNA ligase, RNA fragments with 2’, 3’-cyclic phosphates were covalently attached to defined RNA linkers containing an 8-base long unique molecular identifier (UMI) sequence. Libraries prepared in this manner contain cDNA derived exclusively from RNA fragments with 2', 3'-cyclic phosphates. The UMI sequence allows for detailed quantitation. We optimized and validated 2’, 3’-cyclic phosphate cDNA synthesis and Illumina sequencing methods using viral RNAs cleaved with purified RNase L, viral RNAs cleaved with purified RNase A, and RNA from uninfected and poliovirus-infected HeLa cells.","study_primary_id":"SRP033116"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP033116","sample_accession":"SRS503481","experiment_accession":"SRX378915","run_accession":"SRR1032133","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":false,"study_title":"Ribonuclease L and Metal-Ion-Independent Endoribonuclease Cleavage Sites in Host and Viral RNAs","study_abstract":"We used 2', 3'-cyclic phosphate cDNA synthesis and Illumina sequencing to identify and quantify metal-ion-independent endoribonuclease cleavage sites in host and viral RNAs. Overall design: To make cDNA libraries, we exploited the 2’, 3’-cyclic phosphate at the end of RNA fragments produced by RNase L and other metal-ion-independent endoribonucleases. Using Arabidopsis thaliana tRNA ligase, RNA fragments with 2’, 3’-cyclic phosphates were covalently attached to defined RNA linkers containing an 8-base long unique molecular identifier (UMI) sequence. Libraries prepared in this manner contain cDNA derived exclusively from RNA fragments with 2', 3'-cyclic phosphates. The UMI sequence allows for detailed quantitation. We optimized and validated 2’, 3’-cyclic phosphate cDNA synthesis and Illumina sequencing methods using viral RNAs cleaved with purified RNase L, viral RNAs cleaved with purified RNase A, and RNA from uninfected and poliovirus-infected HeLa cells.","study_primary_id":"SRP033116"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557218","experiment_accession":"SRX469986","run_accession":"SRR1168280","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557206","experiment_accession":"SRX469973","run_accession":"SRR1168267","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557210","experiment_accession":"SRX469978","run_accession":"SRR1168272","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557217","experiment_accession":"SRX469985","run_accession":"SRR1168279","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557207","experiment_accession":"SRX469975","run_accession":"SRR1168269","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557200","experiment_accession":"SRX469968","run_accession":"SRR1168262","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":false,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557215","experiment_accession":"SRX469983","run_accession":"SRR1168277","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557213","experiment_accession":"SRX469981","run_accession":"SRR1168275","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557208","experiment_accession":"SRX469976","run_accession":"SRR1168270","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557223","experiment_accession":"SRX469991","run_accession":"SRR1168285","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557224","experiment_accession":"SRX469992","run_accession":"SRR1168286","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557201","experiment_accession":"SRX469970","run_accession":"SRR1168264","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557199","experiment_accession":"SRX469967","run_accession":"SRR1168261","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557222","experiment_accession":"SRX469990","run_accession":"SRR1168284","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557204","experiment_accession":"SRX469972","run_accession":"SRR1168266","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557221","experiment_accession":"SRX469989","run_accession":"SRR1168283","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557212","experiment_accession":"SRX469980","run_accession":"SRR1168274","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557203","experiment_accession":"SRX469971","run_accession":"SRR1168265","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557205","experiment_accession":"SRX469974","run_accession":"SRR1168268","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557219","experiment_accession":"SRX469987","run_accession":"SRR1168281","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557225","experiment_accession":"SRX469993","run_accession":"SRR1168287","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557220","experiment_accession":"SRX469988","run_accession":"SRR1168282","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557209","experiment_accession":"SRX469977","run_accession":"SRR1168271","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557202","experiment_accession":"SRX469969","run_accession":"SRR1168263","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":false,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557214","experiment_accession":"SRX469982","run_accession":"SRR1168276","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557211","experiment_accession":"SRX469979","run_accession":"SRR1168273","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP037722","sample_accession":"SRS557216","experiment_accession":"SRX469984","run_accession":"SRR1168278","run_center_name":"GEO","machine_type":"Illumina MiSeq","paired_end":true,"study_title":"Deep sequencing shows multiple oligouridylations are required for 3'' to 5'' degradation of histone mRNAs on polyribosomes","study_abstract":"We developed a customized RNA-Seq strategy to identify the 3'' termini of degradation intermediates of histone mRNAs. Using this strategy, we identified two types of oligouridylated degradation intermediates: RNAs ending at different sites of the 3'' side of the stemloop that resulted from initial degradation by 3''hExo and intermediates near the stop codon and within the coding region. We established a method for identifying degradation intermediates for replication-depdendent histone mRNAs. Histone mRNAs are present in large amounts in S-phase cells. Inhibition of DNA replication results in a rapid degradation of histone mRNA. We developed an approach to selectively amplify the 3'' ends of histone mRNA molecules, including degradation intermediates, which we then sequenced. Using a novel bioinformatics platform we identified degradation intermediates including many that had untemplated nts added to the 3'' end. We identified a large variety of degradation intermediates that contained oligo(U) tails. We were able to deduce the 3'' to 5'' pathway of histone mRNA degradation. Overall design: RNA-seq with a custom 3'' linker: The samples analyzed included two biological replicates of RNAs before and 20 min after HU treatment (samples 1, 26, 27) capped RNAs from cells treated with HU for 20 min (samples 2,3,16,17) RNA isolated from polyribosomes 20 min after HU treatment, from untreated cells (samples 4-9) and cells treated with pactamycin for 5 min (samples 10-15); from cells in which the exosome subunit Pml/SC100 had been knocked down (samples 22-23) and cells treated with the control siRNA (samples 20-21). Please note that, for Sample 2 and Sample 3, the sequencer was unable to recover both ends in the mate pairs for these two sequencing runs, but we chose to use these data anyway since the reads that were recovered included the 3'' linker that we used to determine the presence of untemplated additions.","study_primary_id":"SRP037722"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP041466","sample_accession":"SRS598088","experiment_accession":"SRX528179","run_accession":"SRR1264358","run_center_name":"Chinese Academy of Sciences","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Homo sapiens strain:HCT-116 cell lines Exome","study_abstract":"A transcriptome-wide analysis of miRNA-mediated surveillance.","study_primary_id":"SRP041466"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP042630","sample_accession":"SRS624510","experiment_accession":"SRX560111","run_accession":"SRR1313741","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"P493-6 treated with KJ-Pyr-9 and/or Doxycycline","study_abstract":"In a fluorescence polarization screen for MYC-MAX interaction, we have identified a novel small molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine library. The Kd of KJ-Pyr-9 for MYC in vitro is 6.5 ± 1.0 nM as determined by backscattering interferometry; KJ-Pyr-9 also interferes with MYC-MAX complex formation in the cell as shown in a protein fragment complementation assay. KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or only weak effects on the oncogenic activity of several unrelated oncoproteins. KJ-Pyr-9 preferentially interferes with the proliferation of MYC-overexpressing human and avian cells and specifically reduces the MYC-driven transcriptional signature. In vivo, KJ-Pyr-9 effectively blocks the growth of a xenotransplant of MYC-overexpressing  human cancer cells. Overall design: 4 treatment groups analyzed in triplicate: no treatment(control), 20uM KJ-Pyr-9, 0.1ug/mL doxycycline and KJ-Pyr-9 in combination with doxycycline","study_primary_id":"SRP042630"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP042630","sample_accession":"SRS624510","experiment_accession":"SRX560111","run_accession":"SRR1313742","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"P493-6 treated with KJ-Pyr-9 and/or Doxycycline","study_abstract":"In a fluorescence polarization screen for MYC-MAX interaction, we have identified a novel small molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine library. The Kd of KJ-Pyr-9 for MYC in vitro is 6.5 ± 1.0 nM as determined by backscattering interferometry; KJ-Pyr-9 also interferes with MYC-MAX complex formation in the cell as shown in a protein fragment complementation assay. KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or only weak effects on the oncogenic activity of several unrelated oncoproteins. KJ-Pyr-9 preferentially interferes with the proliferation of MYC-overexpressing human and avian cells and specifically reduces the MYC-driven transcriptional signature. In vivo, KJ-Pyr-9 effectively blocks the growth of a xenotransplant of MYC-overexpressing  human cancer cells. Overall design: 4 treatment groups analyzed in triplicate: no treatment(control), 20uM KJ-Pyr-9, 0.1ug/mL doxycycline and KJ-Pyr-9 in combination with doxycycline","study_primary_id":"SRP042630"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP042630","sample_accession":"SRS624510","experiment_accession":"SRX560111","run_accession":"SRR1313743","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"P493-6 treated with KJ-Pyr-9 and/or Doxycycline","study_abstract":"In a fluorescence polarization screen for MYC-MAX interaction, we have identified a novel small molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine library. The Kd of KJ-Pyr-9 for MYC in vitro is 6.5 ± 1.0 nM as determined by backscattering interferometry; KJ-Pyr-9 also interferes with MYC-MAX complex formation in the cell as shown in a protein fragment complementation assay. KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or only weak effects on the oncogenic activity of several unrelated oncoproteins. KJ-Pyr-9 preferentially interferes with the proliferation of MYC-overexpressing human and avian cells and specifically reduces the MYC-driven transcriptional signature. In vivo, KJ-Pyr-9 effectively blocks the growth of a xenotransplant of MYC-overexpressing  human cancer cells. Overall design: 4 treatment groups analyzed in triplicate: no treatment(control), 20uM KJ-Pyr-9, 0.1ug/mL doxycycline and KJ-Pyr-9 in combination with doxycycline","study_primary_id":"SRP042630"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP042630","sample_accession":"SRS624509","experiment_accession":"SRX560110","run_accession":"SRR1313738","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"P493-6 treated with KJ-Pyr-9 and/or Doxycycline","study_abstract":"In a fluorescence polarization screen for MYC-MAX interaction, we have identified a novel small molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine library. The Kd of KJ-Pyr-9 for MYC in vitro is 6.5 ± 1.0 nM as determined by backscattering interferometry; KJ-Pyr-9 also interferes with MYC-MAX complex formation in the cell as shown in a protein fragment complementation assay. KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or only weak effects on the oncogenic activity of several unrelated oncoproteins. KJ-Pyr-9 preferentially interferes with the proliferation of MYC-overexpressing human and avian cells and specifically reduces the MYC-driven transcriptional signature. In vivo, KJ-Pyr-9 effectively blocks the growth of a xenotransplant of MYC-overexpressing  human cancer cells. Overall design: 4 treatment groups analyzed in triplicate: no treatment(control), 20uM KJ-Pyr-9, 0.1ug/mL doxycycline and KJ-Pyr-9 in combination with doxycycline","study_primary_id":"SRP042630"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP042630","sample_accession":"SRS624509","experiment_accession":"SRX560110","run_accession":"SRR1313739","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"P493-6 treated with KJ-Pyr-9 and/or Doxycycline","study_abstract":"In a fluorescence polarization screen for MYC-MAX interaction, we have identified a novel small molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine library. The Kd of KJ-Pyr-9 for MYC in vitro is 6.5 ± 1.0 nM as determined by backscattering interferometry; KJ-Pyr-9 also interferes with MYC-MAX complex formation in the cell as shown in a protein fragment complementation assay. KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or only weak effects on the oncogenic activity of several unrelated oncoproteins. KJ-Pyr-9 preferentially interferes with the proliferation of MYC-overexpressing human and avian cells and specifically reduces the MYC-driven transcriptional signature. In vivo, KJ-Pyr-9 effectively blocks the growth of a xenotransplant of MYC-overexpressing  human cancer cells. Overall design: 4 treatment groups analyzed in triplicate: no treatment(control), 20uM KJ-Pyr-9, 0.1ug/mL doxycycline and KJ-Pyr-9 in combination with doxycycline","study_primary_id":"SRP042630"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP042630","sample_accession":"SRS624509","experiment_accession":"SRX560110","run_accession":"SRR1313740","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"P493-6 treated with KJ-Pyr-9 and/or Doxycycline","study_abstract":"In a fluorescence polarization screen for MYC-MAX interaction, we have identified a novel small molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine library. The Kd of KJ-Pyr-9 for MYC in vitro is 6.5 ± 1.0 nM as determined by backscattering interferometry; KJ-Pyr-9 also interferes with MYC-MAX complex formation in the cell as shown in a protein fragment complementation assay. KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or only weak effects on the oncogenic activity of several unrelated oncoproteins. KJ-Pyr-9 preferentially interferes with the proliferation of MYC-overexpressing human and avian cells and specifically reduces the MYC-driven transcriptional signature. In vivo, KJ-Pyr-9 effectively blocks the growth of a xenotransplant of MYC-overexpressing  human cancer cells. Overall design: 4 treatment groups analyzed in triplicate: no treatment(control), 20uM KJ-Pyr-9, 0.1ug/mL doxycycline and KJ-Pyr-9 in combination with doxycycline","study_primary_id":"SRP042630"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP042630","sample_accession":"SRS624508","experiment_accession":"SRX560109","run_accession":"SRR1313735","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"P493-6 treated with KJ-Pyr-9 and/or Doxycycline","study_abstract":"In a fluorescence polarization screen for MYC-MAX interaction, we have identified a novel small molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine library. The Kd of KJ-Pyr-9 for MYC in vitro is 6.5 ± 1.0 nM as determined by backscattering interferometry; KJ-Pyr-9 also interferes with MYC-MAX complex formation in the cell as shown in a protein fragment complementation assay. KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or only weak effects on the oncogenic activity of several unrelated oncoproteins. KJ-Pyr-9 preferentially interferes with the proliferation of MYC-overexpressing human and avian cells and specifically reduces the MYC-driven transcriptional signature. In vivo, KJ-Pyr-9 effectively blocks the growth of a xenotransplant of MYC-overexpressing  human cancer cells. Overall design: 4 treatment groups analyzed in triplicate: no treatment(control), 20uM KJ-Pyr-9, 0.1ug/mL doxycycline and KJ-Pyr-9 in combination with doxycycline","study_primary_id":"SRP042630"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP042630","sample_accession":"SRS624508","experiment_accession":"SRX560109","run_accession":"SRR1313736","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"P493-6 treated with KJ-Pyr-9 and/or Doxycycline","study_abstract":"In a fluorescence polarization screen for MYC-MAX interaction, we have identified a novel small molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine library. The Kd of KJ-Pyr-9 for MYC in vitro is 6.5 ± 1.0 nM as determined by backscattering interferometry; KJ-Pyr-9 also interferes with MYC-MAX complex formation in the cell as shown in a protein fragment complementation assay. KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or only weak effects on the oncogenic activity of several unrelated oncoproteins. KJ-Pyr-9 preferentially interferes with the proliferation of MYC-overexpressing human and avian cells and specifically reduces the MYC-driven transcriptional signature. In vivo, KJ-Pyr-9 effectively blocks the growth of a xenotransplant of MYC-overexpressing  human cancer cells. Overall design: 4 treatment groups analyzed in triplicate: no treatment(control), 20uM KJ-Pyr-9, 0.1ug/mL doxycycline and KJ-Pyr-9 in combination with doxycycline","study_primary_id":"SRP042630"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP042630","sample_accession":"SRS624508","experiment_accession":"SRX560109","run_accession":"SRR1313737","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"P493-6 treated with KJ-Pyr-9 and/or Doxycycline","study_abstract":"In a fluorescence polarization screen for MYC-MAX interaction, we have identified a novel small molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine library. The Kd of KJ-Pyr-9 for MYC in vitro is 6.5 ± 1.0 nM as determined by backscattering interferometry; KJ-Pyr-9 also interferes with MYC-MAX complex formation in the cell as shown in a protein fragment complementation assay. KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or only weak effects on the oncogenic activity of several unrelated oncoproteins. KJ-Pyr-9 preferentially interferes with the proliferation of MYC-overexpressing human and avian cells and specifically reduces the MYC-driven transcriptional signature. In vivo, KJ-Pyr-9 effectively blocks the growth of a xenotransplant of MYC-overexpressing  human cancer cells. Overall design: 4 treatment groups analyzed in triplicate: no treatment(control), 20uM KJ-Pyr-9, 0.1ug/mL doxycycline and KJ-Pyr-9 in combination with doxycycline","study_primary_id":"SRP042630"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP042630","sample_accession":"SRS624511","experiment_accession":"SRX560112","run_accession":"SRR1313744","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"P493-6 treated with KJ-Pyr-9 and/or Doxycycline","study_abstract":"In a fluorescence polarization screen for MYC-MAX interaction, we have identified a novel small molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine library. The Kd of KJ-Pyr-9 for MYC in vitro is 6.5 ± 1.0 nM as determined by backscattering interferometry; KJ-Pyr-9 also interferes with MYC-MAX complex formation in the cell as shown in a protein fragment complementation assay. KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or only weak effects on the oncogenic activity of several unrelated oncoproteins. KJ-Pyr-9 preferentially interferes with the proliferation of MYC-overexpressing human and avian cells and specifically reduces the MYC-driven transcriptional signature. In vivo, KJ-Pyr-9 effectively blocks the growth of a xenotransplant of MYC-overexpressing  human cancer cells. Overall design: 4 treatment groups analyzed in triplicate: no treatment(control), 20uM KJ-Pyr-9, 0.1ug/mL doxycycline and KJ-Pyr-9 in combination with doxycycline","study_primary_id":"SRP042630"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP042630","sample_accession":"SRS624511","experiment_accession":"SRX560112","run_accession":"SRR1313745","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"P493-6 treated with KJ-Pyr-9 and/or Doxycycline","study_abstract":"In a fluorescence polarization screen for MYC-MAX interaction, we have identified a novel small molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine library. The Kd of KJ-Pyr-9 for MYC in vitro is 6.5 ± 1.0 nM as determined by backscattering interferometry; KJ-Pyr-9 also interferes with MYC-MAX complex formation in the cell as shown in a protein fragment complementation assay. KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or only weak effects on the oncogenic activity of several unrelated oncoproteins. KJ-Pyr-9 preferentially interferes with the proliferation of MYC-overexpressing human and avian cells and specifically reduces the MYC-driven transcriptional signature. In vivo, KJ-Pyr-9 effectively blocks the growth of a xenotransplant of MYC-overexpressing  human cancer cells. Overall design: 4 treatment groups analyzed in triplicate: no treatment(control), 20uM KJ-Pyr-9, 0.1ug/mL doxycycline and KJ-Pyr-9 in combination with doxycycline","study_primary_id":"SRP042630"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP042630","sample_accession":"SRS624511","experiment_accession":"SRX560112","run_accession":"SRR1313746","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"P493-6 treated with KJ-Pyr-9 and/or Doxycycline","study_abstract":"In a fluorescence polarization screen for MYC-MAX interaction, we have identified a novel small molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine library. The Kd of KJ-Pyr-9 for MYC in vitro is 6.5 ± 1.0 nM as determined by backscattering interferometry; KJ-Pyr-9 also interferes with MYC-MAX complex formation in the cell as shown in a protein fragment complementation assay. KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or only weak effects on the oncogenic activity of several unrelated oncoproteins. KJ-Pyr-9 preferentially interferes with the proliferation of MYC-overexpressing human and avian cells and specifically reduces the MYC-driven transcriptional signature. In vivo, KJ-Pyr-9 effectively blocks the growth of a xenotransplant of MYC-overexpressing  human cancer cells. Overall design: 4 treatment groups analyzed in triplicate: no treatment(control), 20uM KJ-Pyr-9, 0.1ug/mL doxycycline and KJ-Pyr-9 in combination with doxycycline","study_primary_id":"SRP042630"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP049004","sample_accession":"SRS722896","experiment_accession":"SRX734471","run_accession":"SRR1614283","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Enhanced MyoD-Induced Transdifferentiation to a Myogenic Lineage by Fusion to a Potent Transactivation Domain","study_abstract":"Synthetic transcription factors can be applied to many areas of biotechnology, medicine, and basic research.  Currently, the most common method for engineering synthetic transcription factors has been based on programmable DNA-binding domains of zinc finger proteins, Transcription Activator-Like Effectors (TALEs), and most recently the CRISPR/Cas9 system. These transcription factor platforms consist of the DNA-binding domain fused to potent transcriptional activation domains, most commonly the tetramer of the minimal transactivation domain of the VP16 protein from herpes simplex virus, referred to as VP64. Although many applications are well-suited for the targeted activation of a single gene, genetic reprogramming requires the coordinated regulation of many nodes of natural gene networks as is typically performed by naturally occurring reprogramming factors. Thus we sought to combine principles from each of these approaches by attaching potent transcriptional activation domains to a natural reprogramming factor to increase the efficiency and/or rate of cell fate conversion. In this study, we evaluated the effects of fusing potent activation domains to the transcription factor MyoD, the master regulator of the skeletal myoblast lineage. In certain non-myogenic lineages, MyoD overexpression causes upregulation of the myogenic gene network and conversion to a myoblast phenotype including cell fusion into multinucleated myotubes. Compared to wild-type MyoD, the VP64-MyoD fusion protein induced greater overall reprogramming of global gene expression. This simple approach for increasing the potency of natural reprogramming factors circumvents the need for screening engineered proteins and leads to a more robust cellular reprogramming compared to treatment with the wild type transcription factor. Overall design: Human dermal fibroblasts were transduced with a single tet inducible lentivirus that expresses either WT-MyoD or VP64-MyoD in response to treatment with doxycycline. Untreated human dermal fibroblast served as the negative control. Gene expression was measured using mRNA-seq, and differential expression was calculated using DESeq. All experiments were performed in biological duplicates.","study_primary_id":"SRP049004"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP049004","sample_accession":"SRS722894","experiment_accession":"SRX734469","run_accession":"SRR1614281","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Enhanced MyoD-Induced Transdifferentiation to a Myogenic Lineage by Fusion to a Potent Transactivation Domain","study_abstract":"Synthetic transcription factors can be applied to many areas of biotechnology, medicine, and basic research.  Currently, the most common method for engineering synthetic transcription factors has been based on programmable DNA-binding domains of zinc finger proteins, Transcription Activator-Like Effectors (TALEs), and most recently the CRISPR/Cas9 system. These transcription factor platforms consist of the DNA-binding domain fused to potent transcriptional activation domains, most commonly the tetramer of the minimal transactivation domain of the VP16 protein from herpes simplex virus, referred to as VP64. Although many applications are well-suited for the targeted activation of a single gene, genetic reprogramming requires the coordinated regulation of many nodes of natural gene networks as is typically performed by naturally occurring reprogramming factors. Thus we sought to combine principles from each of these approaches by attaching potent transcriptional activation domains to a natural reprogramming factor to increase the efficiency and/or rate of cell fate conversion. In this study, we evaluated the effects of fusing potent activation domains to the transcription factor MyoD, the master regulator of the skeletal myoblast lineage. In certain non-myogenic lineages, MyoD overexpression causes upregulation of the myogenic gene network and conversion to a myoblast phenotype including cell fusion into multinucleated myotubes. Compared to wild-type MyoD, the VP64-MyoD fusion protein induced greater overall reprogramming of global gene expression. This simple approach for increasing the potency of natural reprogramming factors circumvents the need for screening engineered proteins and leads to a more robust cellular reprogramming compared to treatment with the wild type transcription factor. Overall design: Human dermal fibroblasts were transduced with a single tet inducible lentivirus that expresses either WT-MyoD or VP64-MyoD in response to treatment with doxycycline. Untreated human dermal fibroblast served as the negative control. Gene expression was measured using mRNA-seq, and differential expression was calculated using DESeq. All experiments were performed in biological duplicates.","study_primary_id":"SRP049004"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP049004","sample_accession":"SRS722897","experiment_accession":"SRX734472","run_accession":"SRR1614284","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Enhanced MyoD-Induced Transdifferentiation to a Myogenic Lineage by Fusion to a Potent Transactivation Domain","study_abstract":"Synthetic transcription factors can be applied to many areas of biotechnology, medicine, and basic research.  Currently, the most common method for engineering synthetic transcription factors has been based on programmable DNA-binding domains of zinc finger proteins, Transcription Activator-Like Effectors (TALEs), and most recently the CRISPR/Cas9 system. These transcription factor platforms consist of the DNA-binding domain fused to potent transcriptional activation domains, most commonly the tetramer of the minimal transactivation domain of the VP16 protein from herpes simplex virus, referred to as VP64. Although many applications are well-suited for the targeted activation of a single gene, genetic reprogramming requires the coordinated regulation of many nodes of natural gene networks as is typically performed by naturally occurring reprogramming factors. Thus we sought to combine principles from each of these approaches by attaching potent transcriptional activation domains to a natural reprogramming factor to increase the efficiency and/or rate of cell fate conversion. In this study, we evaluated the effects of fusing potent activation domains to the transcription factor MyoD, the master regulator of the skeletal myoblast lineage. In certain non-myogenic lineages, MyoD overexpression causes upregulation of the myogenic gene network and conversion to a myoblast phenotype including cell fusion into multinucleated myotubes. Compared to wild-type MyoD, the VP64-MyoD fusion protein induced greater overall reprogramming of global gene expression. This simple approach for increasing the potency of natural reprogramming factors circumvents the need for screening engineered proteins and leads to a more robust cellular reprogramming compared to treatment with the wild type transcription factor. Overall design: Human dermal fibroblasts were transduced with a single tet inducible lentivirus that expresses either WT-MyoD or VP64-MyoD in response to treatment with doxycycline. Untreated human dermal fibroblast served as the negative control. Gene expression was measured using mRNA-seq, and differential expression was calculated using DESeq. All experiments were performed in biological duplicates.","study_primary_id":"SRP049004"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP049004","sample_accession":"SRS722895","experiment_accession":"SRX734470","run_accession":"SRR1614282","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Enhanced MyoD-Induced Transdifferentiation to a Myogenic Lineage by Fusion to a Potent Transactivation Domain","study_abstract":"Synthetic transcription factors can be applied to many areas of biotechnology, medicine, and basic research.  Currently, the most common method for engineering synthetic transcription factors has been based on programmable DNA-binding domains of zinc finger proteins, Transcription Activator-Like Effectors (TALEs), and most recently the CRISPR/Cas9 system. These transcription factor platforms consist of the DNA-binding domain fused to potent transcriptional activation domains, most commonly the tetramer of the minimal transactivation domain of the VP16 protein from herpes simplex virus, referred to as VP64. Although many applications are well-suited for the targeted activation of a single gene, genetic reprogramming requires the coordinated regulation of many nodes of natural gene networks as is typically performed by naturally occurring reprogramming factors. Thus we sought to combine principles from each of these approaches by attaching potent transcriptional activation domains to a natural reprogramming factor to increase the efficiency and/or rate of cell fate conversion. In this study, we evaluated the effects of fusing potent activation domains to the transcription factor MyoD, the master regulator of the skeletal myoblast lineage. In certain non-myogenic lineages, MyoD overexpression causes upregulation of the myogenic gene network and conversion to a myoblast phenotype including cell fusion into multinucleated myotubes. Compared to wild-type MyoD, the VP64-MyoD fusion protein induced greater overall reprogramming of global gene expression. This simple approach for increasing the potency of natural reprogramming factors circumvents the need for screening engineered proteins and leads to a more robust cellular reprogramming compared to treatment with the wild type transcription factor. Overall design: Human dermal fibroblasts were transduced with a single tet inducible lentivirus that expresses either WT-MyoD or VP64-MyoD in response to treatment with doxycycline. Untreated human dermal fibroblast served as the negative control. Gene expression was measured using mRNA-seq, and differential expression was calculated using DESeq. All experiments were performed in biological duplicates.","study_primary_id":"SRP049004"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP049004","sample_accession":"SRS722898","experiment_accession":"SRX734473","run_accession":"SRR1614285","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Enhanced MyoD-Induced Transdifferentiation to a Myogenic Lineage by Fusion to a Potent Transactivation Domain","study_abstract":"Synthetic transcription factors can be applied to many areas of biotechnology, medicine, and basic research.  Currently, the most common method for engineering synthetic transcription factors has been based on programmable DNA-binding domains of zinc finger proteins, Transcription Activator-Like Effectors (TALEs), and most recently the CRISPR/Cas9 system. These transcription factor platforms consist of the DNA-binding domain fused to potent transcriptional activation domains, most commonly the tetramer of the minimal transactivation domain of the VP16 protein from herpes simplex virus, referred to as VP64. Although many applications are well-suited for the targeted activation of a single gene, genetic reprogramming requires the coordinated regulation of many nodes of natural gene networks as is typically performed by naturally occurring reprogramming factors. Thus we sought to combine principles from each of these approaches by attaching potent transcriptional activation domains to a natural reprogramming factor to increase the efficiency and/or rate of cell fate conversion. In this study, we evaluated the effects of fusing potent activation domains to the transcription factor MyoD, the master regulator of the skeletal myoblast lineage. In certain non-myogenic lineages, MyoD overexpression causes upregulation of the myogenic gene network and conversion to a myoblast phenotype including cell fusion into multinucleated myotubes. Compared to wild-type MyoD, the VP64-MyoD fusion protein induced greater overall reprogramming of global gene expression. This simple approach for increasing the potency of natural reprogramming factors circumvents the need for screening engineered proteins and leads to a more robust cellular reprogramming compared to treatment with the wild type transcription factor. Overall design: Human dermal fibroblasts were transduced with a single tet inducible lentivirus that expresses either WT-MyoD or VP64-MyoD in response to treatment with doxycycline. Untreated human dermal fibroblast served as the negative control. Gene expression was measured using mRNA-seq, and differential expression was calculated using DESeq. All experiments were performed in biological duplicates.","study_primary_id":"SRP049004"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP049004","sample_accession":"SRS722893","experiment_accession":"SRX734468","run_accession":"SRR1614280","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Enhanced MyoD-Induced Transdifferentiation to a Myogenic Lineage by Fusion to a Potent Transactivation Domain","study_abstract":"Synthetic transcription factors can be applied to many areas of biotechnology, medicine, and basic research.  Currently, the most common method for engineering synthetic transcription factors has been based on programmable DNA-binding domains of zinc finger proteins, Transcription Activator-Like Effectors (TALEs), and most recently the CRISPR/Cas9 system. These transcription factor platforms consist of the DNA-binding domain fused to potent transcriptional activation domains, most commonly the tetramer of the minimal transactivation domain of the VP16 protein from herpes simplex virus, referred to as VP64. Although many applications are well-suited for the targeted activation of a single gene, genetic reprogramming requires the coordinated regulation of many nodes of natural gene networks as is typically performed by naturally occurring reprogramming factors. Thus we sought to combine principles from each of these approaches by attaching potent transcriptional activation domains to a natural reprogramming factor to increase the efficiency and/or rate of cell fate conversion. In this study, we evaluated the effects of fusing potent activation domains to the transcription factor MyoD, the master regulator of the skeletal myoblast lineage. In certain non-myogenic lineages, MyoD overexpression causes upregulation of the myogenic gene network and conversion to a myoblast phenotype including cell fusion into multinucleated myotubes. Compared to wild-type MyoD, the VP64-MyoD fusion protein induced greater overall reprogramming of global gene expression. This simple approach for increasing the potency of natural reprogramming factors circumvents the need for screening engineered proteins and leads to a more robust cellular reprogramming compared to treatment with the wild type transcription factor. Overall design: Human dermal fibroblasts were transduced with a single tet inducible lentivirus that expresses either WT-MyoD or VP64-MyoD in response to treatment with doxycycline. Untreated human dermal fibroblast served as the negative control. Gene expression was measured using mRNA-seq, and differential expression was calculated using DESeq. All experiments were performed in biological duplicates.","study_primary_id":"SRP049004"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777455","experiment_accession":"SRX803442","run_accession":"SRR1701777","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777454","experiment_accession":"SRX803360","run_accession":"SRR1701435","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777411","experiment_accession":"SRX803377","run_accession":"SRR1701527","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777412","experiment_accession":"SRX803289","run_accession":"SRR1701153","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777354","experiment_accession":"SRX803415","run_accession":"SRR1701687","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777377","experiment_accession":"SRX803319","run_accession":"SRR1701256","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777449","experiment_accession":"SRX803282","run_accession":"SRR1701117","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777442","experiment_accession":"SRX803301","run_accession":"SRR1701197","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777397","experiment_accession":"SRX803445","run_accession":"SRR1701796","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777415","experiment_accession":"SRX803409","run_accession":"SRR1701662","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777475","experiment_accession":"SRX803379","run_accession":"SRR1701556","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777365","experiment_accession":"SRX803368","run_accession":"SRR1701473","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777347","experiment_accession":"SRX803352","run_accession":"SRR1701405","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777426","experiment_accession":"SRX803404","run_accession":"SRR1701638","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777448","experiment_accession":"SRX803375","run_accession":"SRR1701511","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777423","experiment_accession":"SRX803287","run_accession":"SRR1701137","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777464","experiment_accession":"SRX803335","run_accession":"SRR1701327","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777465","experiment_accession":"SRX803336","run_accession":"SRR1701343","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777456","experiment_accession":"SRX803447","run_accession":"SRR1701812","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777441","experiment_accession":"SRX803321","run_accession":"SRR1701272","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777368","experiment_accession":"SRX803432","run_accession":"SRR1701742","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777460","experiment_accession":"SRX803324","run_accession":"SRR1701291","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777471","experiment_accession":"SRX803304","run_accession":"SRR1701216","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777435","experiment_accession":"SRX803370","run_accession":"SRR1701489","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777348","experiment_accession":"SRX803394","run_accession":"SRR1701598","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777416","experiment_accession":"SRX803403","run_accession":"SRR1701622","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777425","experiment_accession":"SRX803422","run_accession":"SRR1701708","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777360","experiment_accession":"SRX803327","run_accession":"SRR1701307","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777370","experiment_accession":"SRX803364","run_accession":"SRR1701454","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777405","experiment_accession":"SRX803343","run_accession":"SRR1701369","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777436","experiment_accession":"SRX803293","run_accession":"SRR1701172","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777399","experiment_accession":"SRX803277","run_accession":"SRR1701090","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777390","experiment_accession":"SRX803279","run_accession":"SRR1701102","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777458","experiment_accession":"SRX803449","run_accession":"SRR1701828","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP050453","sample_accession":"SRS777393","experiment_accession":"SRX803387","run_accession":"SRR1701572","run_center_name":"BI","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Osteosarcoma Genomics","study_abstract":"In this study we attempt to elucidate the genomic characteristics of osteosarcoma. Clinical characteristics. 58 tumor / normal pairs from 58 patients were included in the study. Median age at diagnosis was 12 years. 49% of the patients were male and 47% had metastases at diagnosis. 5 year overall survival was 49% for the entire population, 33% for patients with metastatic disease and 64% for patients with localized disease. Patients with metastatic disease at diagnosis had a significantly worse overall survival. All cases except 2 were sporadic and no patients had stigmata of Rothmund-Thomson, Bloom''s or Werner''s syndromes or Paget''s disease. Two familial cases were affected siblings from a family in which there were 2 unaffected parents and 2 unaffected siblings. None of the patients had known Li Fraumeni or hereditary retinoblastoma. Sample Selection and Clinical Data. Samples were contributed by hospitals in Brazil, Spain, Mexico and the United... (for more see dbGaP study page.)","study_primary_id":"SRP050453"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP055770","sample_accession":"SRS861673","experiment_accession":"SRX895872","run_accession":"SRR1824492","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA","study_abstract":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA. Overall design: Nuclei from three biological replicates were isolated by detergent lysis, fractionated, then three chromatin and three soluble RNA samples were converted to cDNA using Illumina TruSeq stranded protocol, and sequenced on Illumina HiSeq2000","study_primary_id":"SRP055770"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP055770","sample_accession":"SRS861672","experiment_accession":"SRX895873","run_accession":"SRR1824493","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA","study_abstract":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA. Overall design: Nuclei from three biological replicates were isolated by detergent lysis, fractionated, then three chromatin and three soluble RNA samples were converted to cDNA using Illumina TruSeq stranded protocol, and sequenced on Illumina HiSeq2000","study_primary_id":"SRP055770"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP055770","sample_accession":"SRS861666","experiment_accession":"SRX895879","run_accession":"SRR1824499","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA","study_abstract":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA. Overall design: Nuclei from three biological replicates were isolated by detergent lysis, fractionated, then three chromatin and three soluble RNA samples were converted to cDNA using Illumina TruSeq stranded protocol, and sequenced on Illumina HiSeq2000","study_primary_id":"SRP055770"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP055770","sample_accession":"SRS861665","experiment_accession":"SRX895880","run_accession":"SRR1824500","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA","study_abstract":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA. Overall design: Nuclei from three biological replicates were isolated by detergent lysis, fractionated, then three chromatin and three soluble RNA samples were converted to cDNA using Illumina TruSeq stranded protocol, and sequenced on Illumina HiSeq2000","study_primary_id":"SRP055770"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP055770","sample_accession":"SRS861664","experiment_accession":"SRX895881","run_accession":"SRR1824501","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA","study_abstract":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA. Overall design: Nuclei from three biological replicates were isolated by detergent lysis, fractionated, then three chromatin and three soluble RNA samples were converted to cDNA using Illumina TruSeq stranded protocol, and sequenced on Illumina HiSeq2000","study_primary_id":"SRP055770"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP055770","sample_accession":"SRS861668","experiment_accession":"SRX895877","run_accession":"SRR1824497","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA","study_abstract":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA. Overall design: Nuclei from three biological replicates were isolated by detergent lysis, fractionated, then three chromatin and three soluble RNA samples were converted to cDNA using Illumina TruSeq stranded protocol, and sequenced on Illumina HiSeq2000","study_primary_id":"SRP055770"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP055770","sample_accession":"SRS861667","experiment_accession":"SRX895878","run_accession":"SRR1824498","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA","study_abstract":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA. Overall design: Nuclei from three biological replicates were isolated by detergent lysis, fractionated, then three chromatin and three soluble RNA samples were converted to cDNA using Illumina TruSeq stranded protocol, and sequenced on Illumina HiSeq2000","study_primary_id":"SRP055770"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP055770","sample_accession":"SRS861670","experiment_accession":"SRX895875","run_accession":"SRR1824495","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA","study_abstract":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA. Overall design: Nuclei from three biological replicates were isolated by detergent lysis, fractionated, then three chromatin and three soluble RNA samples were converted to cDNA using Illumina TruSeq stranded protocol, and sequenced on Illumina HiSeq2000","study_primary_id":"SRP055770"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP055770","sample_accession":"SRS861671","experiment_accession":"SRX895874","run_accession":"SRR1824494","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA","study_abstract":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA. Overall design: Nuclei from three biological replicates were isolated by detergent lysis, fractionated, then three chromatin and three soluble RNA samples were converted to cDNA using Illumina TruSeq stranded protocol, and sequenced on Illumina HiSeq2000","study_primary_id":"SRP055770"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP055770","sample_accession":"SRS861669","experiment_accession":"SRX895876","run_accession":"SRR1824496","run_center_name":"GEO","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA","study_abstract":"Biochemical fractionation of HEK293 nuclei and RNA-seq of chromatin-associated and soluble-nuclear RNA. Overall design: Nuclei from three biological replicates were isolated by detergent lysis, fractionated, then three chromatin and three soluble RNA samples were converted to cDNA using Illumina TruSeq stranded protocol, and sequenced on Illumina HiSeq2000","study_primary_id":"SRP055770"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979188","experiment_accession":"SRX1081292","run_accession":"SRR2087297","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979157","experiment_accession":"SRX1081323","run_accession":"SRR2087328","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979178","experiment_accession":"SRX1081301","run_accession":"SRR2087306","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979132","experiment_accession":"SRX1081348","run_accession":"SRR2087353","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979189","experiment_accession":"SRX1081291","run_accession":"SRR2087286","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979113","experiment_accession":"SRX1081367","run_accession":"SRR2087372","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979119","experiment_accession":"SRX1081361","run_accession":"SRR2087366","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979127","experiment_accession":"SRX1081353","run_accession":"SRR2087358","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979130","experiment_accession":"SRX1081350","run_accession":"SRR2087355","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979143","experiment_accession":"SRX1081337","run_accession":"SRR2087342","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979203","experiment_accession":"SRX1081277","run_accession":"SRR2087282","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979135","experiment_accession":"SRX1081345","run_accession":"SRR2087350","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979139","experiment_accession":"SRX1081341","run_accession":"SRR2087346","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979121","experiment_accession":"SRX1081359","run_accession":"SRR2087364","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979141","experiment_accession":"SRX1081339","run_accession":"SRR2087344","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979124","experiment_accession":"SRX1081356","run_accession":"SRR2087361","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979115","experiment_accession":"SRX1081365","run_accession":"SRR2087370","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979171","experiment_accession":"SRX1081309","run_accession":"SRR2087314","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979186","experiment_accession":"SRX1081294","run_accession":"SRR2087299","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979187","experiment_accession":"SRX1081293","run_accession":"SRR2087298","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979200","experiment_accession":"SRX1081280","run_accession":"SRR2087289","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979175","experiment_accession":"SRX1081305","run_accession":"SRR2087310","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979151","experiment_accession":"SRX1081329","run_accession":"SRR2087334","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979201","experiment_accession":"SRX1081279","run_accession":"SRR2087288","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979120","experiment_accession":"SRX1081360","run_accession":"SRR2087365","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979156","experiment_accession":"SRX1081324","run_accession":"SRR2087329","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979181","experiment_accession":"SRX1081299","run_accession":"SRR2087304","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979138","experiment_accession":"SRX1081342","run_accession":"SRR2087347","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979183","experiment_accession":"SRX1081298","run_accession":"SRR2087303","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979137","experiment_accession":"SRX1081343","run_accession":"SRR2087348","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979182","experiment_accession":"SRX1081297","run_accession":"SRR2087302","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979169","experiment_accession":"SRX1081310","run_accession":"SRR2087315","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979160","experiment_accession":"SRX1081320","run_accession":"SRR2087325","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979154","experiment_accession":"SRX1081326","run_accession":"SRR2087331","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979172","experiment_accession":"SRX1081307","run_accession":"SRR2087312","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979117","experiment_accession":"SRX1081363","run_accession":"SRR2087368","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979142","experiment_accession":"SRX1081338","run_accession":"SRR2087343","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979177","experiment_accession":"SRX1081302","run_accession":"SRR2087307","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979168","experiment_accession":"SRX1081312","run_accession":"SRR2087317","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979174","experiment_accession":"SRX1081306","run_accession":"SRR2087311","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979110","experiment_accession":"SRX1081370","run_accession":"SRR2087375","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979196","experiment_accession":"SRX1081284","run_accession":"SRR2087293","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979118","experiment_accession":"SRX1081362","run_accession":"SRR2087367","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979126","experiment_accession":"SRX1081354","run_accession":"SRR2087359","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979170","experiment_accession":"SRX1081311","run_accession":"SRR2087316","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979195","experiment_accession":"SRX1081285","run_accession":"SRR2087294","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979149","experiment_accession":"SRX1081330","run_accession":"SRR2087335","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979184","experiment_accession":"SRX1081296","run_accession":"SRR2087301","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979158","experiment_accession":"SRX1081322","run_accession":"SRR2087327","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979162","experiment_accession":"SRX1081318","run_accession":"SRR2087323","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979173","experiment_accession":"SRX1081308","run_accession":"SRR2087313","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979123","experiment_accession":"SRX1081357","run_accession":"SRR2087362","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979176","experiment_accession":"SRX1081303","run_accession":"SRR2087308","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979199","experiment_accession":"SRX1081281","run_accession":"SRR2087290","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979145","experiment_accession":"SRX1081335","run_accession":"SRR2087340","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979194","experiment_accession":"SRX1081286","run_accession":"SRR2087295","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979197","experiment_accession":"SRX1081283","run_accession":"SRR2087292","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979114","experiment_accession":"SRX1081366","run_accession":"SRR2087371","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979161","experiment_accession":"SRX1081319","run_accession":"SRR2087324","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979164","experiment_accession":"SRX1081316","run_accession":"SRR2087321","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979190","experiment_accession":"SRX1081290","run_accession":"SRR2087285","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979185","experiment_accession":"SRX1081295","run_accession":"SRR2087300","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979144","experiment_accession":"SRX1081336","run_accession":"SRR2087341","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979136","experiment_accession":"SRX1081344","run_accession":"SRR2087349","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979153","experiment_accession":"SRX1081327","run_accession":"SRR2087332","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979165","experiment_accession":"SRX1081315","run_accession":"SRR2087320","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979179","experiment_accession":"SRX1081304","run_accession":"SRR2087309","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979152","experiment_accession":"SRX1081328","run_accession":"SRR2087333","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979122","experiment_accession":"SRX1081358","run_accession":"SRR2087363","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979140","experiment_accession":"SRX1081340","run_accession":"SRR2087345","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979128","experiment_accession":"SRX1081352","run_accession":"SRR2087357","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979129","experiment_accession":"SRX1081351","run_accession":"SRR2087356","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979131","experiment_accession":"SRX1081349","run_accession":"SRR2087354","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979146","experiment_accession":"SRX1081334","run_accession":"SRR2087339","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979167","experiment_accession":"SRX1081313","run_accession":"SRR2087318","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979193","experiment_accession":"SRX1081287","run_accession":"SRR2087296","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979159","experiment_accession":"SRX1081321","run_accession":"SRR2087326","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979116","experiment_accession":"SRX1081364","run_accession":"SRR2087369","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979202","experiment_accession":"SRX1081278","run_accession":"SRR2087287","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979166","experiment_accession":"SRX1081314","run_accession":"SRR2087319","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979192","experiment_accession":"SRX1081288","run_accession":"SRR2087283","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979191","experiment_accession":"SRX1081289","run_accession":"SRR2087284","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979111","experiment_accession":"SRX1081369","run_accession":"SRR2087374","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979134","experiment_accession":"SRX1081346","run_accession":"SRR2087351","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979112","experiment_accession":"SRX1081368","run_accession":"SRR2087373","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979148","experiment_accession":"SRX1081332","run_accession":"SRR2087337","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979155","experiment_accession":"SRX1081325","run_accession":"SRR2087330","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979198","experiment_accession":"SRX1081282","run_accession":"SRR2087291","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979133","experiment_accession":"SRX1081347","run_accession":"SRR2087352","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979150","experiment_accession":"SRX1081331","run_accession":"SRR2087336","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979125","experiment_accession":"SRX1081355","run_accession":"SRR2087360","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979147","experiment_accession":"SRX1081333","run_accession":"SRR2087338","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979180","experiment_accession":"SRX1081300","run_accession":"SRR2087305","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP060355","sample_accession":"SRS979163","experiment_accession":"SRX1081317","run_accession":"SRR2087322","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptomic variation of pharmacogenes in multiple human tissues and lymphoblastoid cell lines","study_abstract":"Variation in the expression level and activity of genes involved in drug disposition and action (“pharmacogenes”) can affect drug response and toxicity, especially when in tissues of pharmacological importance. Previous studies have relied primarily on microarrays to understand gene expression differences, or have focused on a single tissue or small number of samples. The goal of this study was to use RNA-seq to determine the expression levels and alternative splicing of 389 PGRN pharmacogenes across four tissues (liver, kidney, heart and adipose) and lymphoblastoid cell lines (LCLs), which are used widely in pharmacogenomics studies. Analysis of RNA-seq data from different individuals across the 5 tissues (N = 139 samples) revealed substantial variation in both expression levels and splicing across samples and tissue types. This in-depth exploration also revealed 183 splicing events in pharmacogenes that were previously not annotated. Overall, this study serves as a rich resource for the research community to inform biomarker and drug discovery and use. Overall design: mRNA profile of 389 genes in 24 liver, 20 kidney (cortex), 25 heart (left ventricle), 25 adipose (subcutaneous) samples, and 45 lymphoblastoid cell lines (LCLs). The raw data for the LCL Samples will be available through dbGap under phs000481.","study_primary_id":"SRP060355"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066895","sample_accession":"SRS1186101","experiment_accession":"SRX1458638","run_accession":"SRR2969257","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Gene expression profiles in NORAD knockout and PUMILIO overexpressing cells","study_abstract":"Purpose: PUMILIO proteins are known to repress target genes by specifically binding to PUMILIO response elements (PREs) in target mRNAs. NORAD is a noncoding RNA that negatively regulates PUMILIO activity. The goal of this study was to determine the gene expression changes that result from knockout of NORAD or overexpression of PUMILIO and to test whether NORAD knockout causes PUMILIO hyperactivity. Methods: RNA-seq libraries were prepared using the TruSeq Stranded Total RNA with Ribo-Zero Human/Mouse/Rat Sample Preparation kit (Illumina) and sequenced using the 100 bp paired-end protocol on an Illumina HiSeq 2000. For comparing NORAD+/+ and NORAD-/- HCT116 cells, 3 biological replicates per genotype were sequenced. For PUM overexpression experiments, 3 replicates of GFP-expressing HCT116 cells (negative control) and 2 independent PUM1- or PUM2-overexpressing clones (2 replicates each) were sequenced. Results: Gene expression profiles show that PUMILIO target genes are downregulated in both NORAD knockout cells and PUMILIO overexpressing cells. Conclusions: These data indicate that NORAD sequesters PUMILIO, preventing excessive repression of PUMILIO target genes that are important for maintaining genomic stability. Overall design: Gene expression profiles of genetically modified HCT116 cells were determined by RNA-seq.","study_primary_id":"SRP066895"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066895","sample_accession":"SRS1186108","experiment_accession":"SRX1458633","run_accession":"SRR2969252","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Gene expression profiles in NORAD knockout and PUMILIO overexpressing cells","study_abstract":"Purpose: PUMILIO proteins are known to repress target genes by specifically binding to PUMILIO response elements (PREs) in target mRNAs. NORAD is a noncoding RNA that negatively regulates PUMILIO activity. The goal of this study was to determine the gene expression changes that result from knockout of NORAD or overexpression of PUMILIO and to test whether NORAD knockout causes PUMILIO hyperactivity. Methods: RNA-seq libraries were prepared using the TruSeq Stranded Total RNA with Ribo-Zero Human/Mouse/Rat Sample Preparation kit (Illumina) and sequenced using the 100 bp paired-end protocol on an Illumina HiSeq 2000. For comparing NORAD+/+ and NORAD-/- HCT116 cells, 3 biological replicates per genotype were sequenced. For PUM overexpression experiments, 3 replicates of GFP-expressing HCT116 cells (negative control) and 2 independent PUM1- or PUM2-overexpressing clones (2 replicates each) were sequenced. Results: Gene expression profiles show that PUMILIO target genes are downregulated in both NORAD knockout cells and PUMILIO overexpressing cells. Conclusions: These data indicate that NORAD sequesters PUMILIO, preventing excessive repression of PUMILIO target genes that are important for maintaining genomic stability. Overall design: Gene expression profiles of genetically modified HCT116 cells were determined by RNA-seq.","study_primary_id":"SRP066895"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066895","sample_accession":"SRS1186111","experiment_accession":"SRX1458631","run_accession":"SRR2969250","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Gene expression profiles in NORAD knockout and PUMILIO overexpressing cells","study_abstract":"Purpose: PUMILIO proteins are known to repress target genes by specifically binding to PUMILIO response elements (PREs) in target mRNAs. NORAD is a noncoding RNA that negatively regulates PUMILIO activity. The goal of this study was to determine the gene expression changes that result from knockout of NORAD or overexpression of PUMILIO and to test whether NORAD knockout causes PUMILIO hyperactivity. Methods: RNA-seq libraries were prepared using the TruSeq Stranded Total RNA with Ribo-Zero Human/Mouse/Rat Sample Preparation kit (Illumina) and sequenced using the 100 bp paired-end protocol on an Illumina HiSeq 2000. For comparing NORAD+/+ and NORAD-/- HCT116 cells, 3 biological replicates per genotype were sequenced. For PUM overexpression experiments, 3 replicates of GFP-expressing HCT116 cells (negative control) and 2 independent PUM1- or PUM2-overexpressing clones (2 replicates each) were sequenced. Results: Gene expression profiles show that PUMILIO target genes are downregulated in both NORAD knockout cells and PUMILIO overexpressing cells. Conclusions: These data indicate that NORAD sequesters PUMILIO, preventing excessive repression of PUMILIO target genes that are important for maintaining genomic stability. Overall design: Gene expression profiles of genetically modified HCT116 cells were determined by RNA-seq.","study_primary_id":"SRP066895"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066895","sample_accession":"SRS1186106","experiment_accession":"SRX1458643","run_accession":"SRR2969262","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Gene expression profiles in NORAD knockout and PUMILIO overexpressing cells","study_abstract":"Purpose: PUMILIO proteins are known to repress target genes by specifically binding to PUMILIO response elements (PREs) in target mRNAs. NORAD is a noncoding RNA that negatively regulates PUMILIO activity. The goal of this study was to determine the gene expression changes that result from knockout of NORAD or overexpression of PUMILIO and to test whether NORAD knockout causes PUMILIO hyperactivity. Methods: RNA-seq libraries were prepared using the TruSeq Stranded Total RNA with Ribo-Zero Human/Mouse/Rat Sample Preparation kit (Illumina) and sequenced using the 100 bp paired-end protocol on an Illumina HiSeq 2000. For comparing NORAD+/+ and NORAD-/- HCT116 cells, 3 biological replicates per genotype were sequenced. For PUM overexpression experiments, 3 replicates of GFP-expressing HCT116 cells (negative control) and 2 independent PUM1- or PUM2-overexpressing clones (2 replicates each) were sequenced. Results: Gene expression profiles show that PUMILIO target genes are downregulated in both NORAD knockout cells and PUMILIO overexpressing cells. Conclusions: These data indicate that NORAD sequesters PUMILIO, preventing excessive repression of PUMILIO target genes that are important for maintaining genomic stability. Overall design: Gene expression profiles of genetically modified HCT116 cells were determined by RNA-seq.","study_primary_id":"SRP066895"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066895","sample_accession":"SRS1186113","experiment_accession":"SRX1458629","run_accession":"SRR2969248","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Gene expression profiles in NORAD knockout and PUMILIO overexpressing cells","study_abstract":"Purpose: PUMILIO proteins are known to repress target genes by specifically binding to PUMILIO response elements (PREs) in target mRNAs. NORAD is a noncoding RNA that negatively regulates PUMILIO activity. The goal of this study was to determine the gene expression changes that result from knockout of NORAD or overexpression of PUMILIO and to test whether NORAD knockout causes PUMILIO hyperactivity. Methods: RNA-seq libraries were prepared using the TruSeq Stranded Total RNA with Ribo-Zero Human/Mouse/Rat Sample Preparation kit (Illumina) and sequenced using the 100 bp paired-end protocol on an Illumina HiSeq 2000. For comparing NORAD+/+ and NORAD-/- HCT116 cells, 3 biological replicates per genotype were sequenced. For PUM overexpression experiments, 3 replicates of GFP-expressing HCT116 cells (negative control) and 2 independent PUM1- or PUM2-overexpressing clones (2 replicates each) were sequenced. Results: Gene expression profiles show that PUMILIO target genes are downregulated in both NORAD knockout cells and PUMILIO overexpressing cells. Conclusions: These data indicate that NORAD sequesters PUMILIO, preventing excessive repression of PUMILIO target genes that are important for maintaining genomic stability. Overall design: Gene expression profiles of genetically modified HCT116 cells were determined by RNA-seq.","study_primary_id":"SRP066895"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066895","sample_accession":"SRS1186110","experiment_accession":"SRX1458642","run_accession":"SRR2969261","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Gene expression profiles in NORAD knockout and PUMILIO overexpressing cells","study_abstract":"Purpose: PUMILIO proteins are known to repress target genes by specifically binding to PUMILIO response elements (PREs) in target mRNAs. NORAD is a noncoding RNA that negatively regulates PUMILIO activity. The goal of this study was to determine the gene expression changes that result from knockout of NORAD or overexpression of PUMILIO and to test whether NORAD knockout causes PUMILIO hyperactivity. Methods: RNA-seq libraries were prepared using the TruSeq Stranded Total RNA with Ribo-Zero Human/Mouse/Rat Sample Preparation kit (Illumina) and sequenced using the 100 bp paired-end protocol on an Illumina HiSeq 2000. For comparing NORAD+/+ and NORAD-/- HCT116 cells, 3 biological replicates per genotype were sequenced. For PUM overexpression experiments, 3 replicates of GFP-expressing HCT116 cells (negative control) and 2 independent PUM1- or PUM2-overexpressing clones (2 replicates each) were sequenced. Results: Gene expression profiles show that PUMILIO target genes are downregulated in both NORAD knockout cells and PUMILIO overexpressing cells. Conclusions: These data indicate that NORAD sequesters PUMILIO, preventing excessive repression of PUMILIO target genes that are important for maintaining genomic stability. Overall design: Gene expression profiles of genetically modified HCT116 cells were determined by RNA-seq.","study_primary_id":"SRP066895"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066895","sample_accession":"SRS1186103","experiment_accession":"SRX1458636","run_accession":"SRR2969255","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Gene expression profiles in NORAD knockout and PUMILIO overexpressing cells","study_abstract":"Purpose: PUMILIO proteins are known to repress target genes by specifically binding to PUMILIO response elements (PREs) in target mRNAs. NORAD is a noncoding RNA that negatively regulates PUMILIO activity. The goal of this study was to determine the gene expression changes that result from knockout of NORAD or overexpression of PUMILIO and to test whether NORAD knockout causes PUMILIO hyperactivity. Methods: RNA-seq libraries were prepared using the TruSeq Stranded Total RNA with Ribo-Zero Human/Mouse/Rat Sample Preparation kit (Illumina) and sequenced using the 100 bp paired-end protocol on an Illumina HiSeq 2000. For comparing NORAD+/+ and NORAD-/- HCT116 cells, 3 biological replicates per genotype were sequenced. For PUM overexpression experiments, 3 replicates of GFP-expressing HCT116 cells (negative control) and 2 independent PUM1- or PUM2-overexpressing clones (2 replicates each) were sequenced. Results: Gene expression profiles show that PUMILIO target genes are downregulated in both NORAD knockout cells and PUMILIO overexpressing cells. Conclusions: These data indicate that NORAD sequesters PUMILIO, preventing excessive repression of PUMILIO target genes that are important for maintaining genomic stability. Overall design: Gene expression profiles of genetically modified HCT116 cells were determined by RNA-seq.","study_primary_id":"SRP066895"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066895","sample_accession":"SRS1186102","experiment_accession":"SRX1458637","run_accession":"SRR2969256","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Gene expression profiles in NORAD knockout and PUMILIO overexpressing cells","study_abstract":"Purpose: PUMILIO proteins are known to repress target genes by specifically binding to PUMILIO response elements (PREs) in target mRNAs. NORAD is a noncoding RNA that negatively regulates PUMILIO activity. The goal of this study was to determine the gene expression changes that result from knockout of NORAD or overexpression of PUMILIO and to test whether NORAD knockout causes PUMILIO hyperactivity. Methods: RNA-seq libraries were prepared using the TruSeq Stranded Total RNA with Ribo-Zero Human/Mouse/Rat Sample Preparation kit (Illumina) and sequenced using the 100 bp paired-end protocol on an Illumina HiSeq 2000. For comparing NORAD+/+ and NORAD-/- HCT116 cells, 3 biological replicates per genotype were sequenced. For PUM overexpression experiments, 3 replicates of GFP-expressing HCT116 cells (negative control) and 2 independent PUM1- or PUM2-overexpressing clones (2 replicates each) were sequenced. Results: Gene expression profiles show that PUMILIO target genes are downregulated in both NORAD knockout cells and PUMILIO overexpressing cells. Conclusions: These data indicate that NORAD sequesters PUMILIO, preventing excessive repression of PUMILIO target genes that are important for maintaining genomic stability. Overall design: Gene expression profiles of genetically modified HCT116 cells were determined by RNA-seq.","study_primary_id":"SRP066895"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066895","sample_accession":"SRS1186104","experiment_accession":"SRX1458635","run_accession":"SRR2969254","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Gene expression profiles in NORAD knockout and PUMILIO overexpressing cells","study_abstract":"Purpose: PUMILIO proteins are known to repress target genes by specifically binding to PUMILIO response elements (PREs) in target mRNAs. NORAD is a noncoding RNA that negatively regulates PUMILIO activity. The goal of this study was to determine the gene expression changes that result from knockout of NORAD or overexpression of PUMILIO and to test whether NORAD knockout causes PUMILIO hyperactivity. Methods: RNA-seq libraries were prepared using the TruSeq Stranded Total RNA with Ribo-Zero Human/Mouse/Rat Sample Preparation kit (Illumina) and sequenced using the 100 bp paired-end protocol on an Illumina HiSeq 2000. For comparing NORAD+/+ and NORAD-/- HCT116 cells, 3 biological replicates per genotype were sequenced. For PUM overexpression experiments, 3 replicates of GFP-expressing HCT116 cells (negative control) and 2 independent PUM1- or PUM2-overexpressing clones (2 replicates each) were sequenced. Results: Gene expression profiles show that PUMILIO target genes are downregulated in both NORAD knockout cells and PUMILIO overexpressing cells. Conclusions: These data indicate that NORAD sequesters PUMILIO, preventing excessive repression of PUMILIO target genes that are important for maintaining genomic stability. Overall design: Gene expression profiles of genetically modified HCT116 cells were determined by RNA-seq.","study_primary_id":"SRP066895"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066895","sample_accession":"SRS1186114","experiment_accession":"SRX1458628","run_accession":"SRR2969247","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Gene expression profiles in NORAD knockout and PUMILIO overexpressing cells","study_abstract":"Purpose: PUMILIO proteins are known to repress target genes by specifically binding to PUMILIO response elements (PREs) in target mRNAs. NORAD is a noncoding RNA that negatively regulates PUMILIO activity. The goal of this study was to determine the gene expression changes that result from knockout of NORAD or overexpression of PUMILIO and to test whether NORAD knockout causes PUMILIO hyperactivity. Methods: RNA-seq libraries were prepared using the TruSeq Stranded Total RNA with Ribo-Zero Human/Mouse/Rat Sample Preparation kit (Illumina) and sequenced using the 100 bp paired-end protocol on an Illumina HiSeq 2000. For comparing NORAD+/+ and NORAD-/- HCT116 cells, 3 biological replicates per genotype were sequenced. For PUM overexpression experiments, 3 replicates of GFP-expressing HCT116 cells (negative control) and 2 independent PUM1- or PUM2-overexpressing clones (2 replicates each) were sequenced. Results: Gene expression profiles show that PUMILIO target genes are downregulated in both NORAD knockout cells and PUMILIO overexpressing cells. Conclusions: These data indicate that NORAD sequesters PUMILIO, preventing excessive repression of PUMILIO target genes that are important for maintaining genomic stability. Overall design: Gene expression profiles of genetically modified HCT116 cells were determined by RNA-seq.","study_primary_id":"SRP066895"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066895","sample_accession":"SRS1186112","experiment_accession":"SRX1458630","run_accession":"SRR2969249","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Gene expression profiles in NORAD knockout and PUMILIO overexpressing cells","study_abstract":"Purpose: PUMILIO proteins are known to repress target genes by specifically binding to PUMILIO response elements (PREs) in target mRNAs. NORAD is a noncoding RNA that negatively regulates PUMILIO activity. The goal of this study was to determine the gene expression changes that result from knockout of NORAD or overexpression of PUMILIO and to test whether NORAD knockout causes PUMILIO hyperactivity. Methods: RNA-seq libraries were prepared using the TruSeq Stranded Total RNA with Ribo-Zero Human/Mouse/Rat Sample Preparation kit (Illumina) and sequenced using the 100 bp paired-end protocol on an Illumina HiSeq 2000. For comparing NORAD+/+ and NORAD-/- HCT116 cells, 3 biological replicates per genotype were sequenced. For PUM overexpression experiments, 3 replicates of GFP-expressing HCT116 cells (negative control) and 2 independent PUM1- or PUM2-overexpressing clones (2 replicates each) were sequenced. Results: Gene expression profiles show that PUMILIO target genes are downregulated in both NORAD knockout cells and PUMILIO overexpressing cells. Conclusions: These data indicate that NORAD sequesters PUMILIO, preventing excessive repression of PUMILIO target genes that are important for maintaining genomic stability. Overall design: Gene expression profiles of genetically modified HCT116 cells were determined by RNA-seq.","study_primary_id":"SRP066895"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066895","sample_accession":"SRS1186100","experiment_accession":"SRX1458639","run_accession":"SRR2969258","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Gene expression profiles in NORAD knockout and PUMILIO overexpressing cells","study_abstract":"Purpose: PUMILIO proteins are known to repress target genes by specifically binding to PUMILIO response elements (PREs) in target mRNAs. NORAD is a noncoding RNA that negatively regulates PUMILIO activity. The goal of this study was to determine the gene expression changes that result from knockout of NORAD or overexpression of PUMILIO and to test whether NORAD knockout causes PUMILIO hyperactivity. Methods: RNA-seq libraries were prepared using the TruSeq Stranded Total RNA with Ribo-Zero Human/Mouse/Rat Sample Preparation kit (Illumina) and sequenced using the 100 bp paired-end protocol on an Illumina HiSeq 2000. For comparing NORAD+/+ and NORAD-/- HCT116 cells, 3 biological replicates per genotype were sequenced. For PUM overexpression experiments, 3 replicates of GFP-expressing HCT116 cells (negative control) and 2 independent PUM1- or PUM2-overexpressing clones (2 replicates each) were sequenced. Results: Gene expression profiles show that PUMILIO target genes are downregulated in both NORAD knockout cells and PUMILIO overexpressing cells. Conclusions: These data indicate that NORAD sequesters PUMILIO, preventing excessive repression of PUMILIO target genes that are important for maintaining genomic stability. Overall design: Gene expression profiles of genetically modified HCT116 cells were determined by RNA-seq.","study_primary_id":"SRP066895"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066895","sample_accession":"SRS1186105","experiment_accession":"SRX1458644","run_accession":"SRR2969263","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Gene expression profiles in NORAD knockout and PUMILIO overexpressing cells","study_abstract":"Purpose: PUMILIO proteins are known to repress target genes by specifically binding to PUMILIO response elements (PREs) in target mRNAs. NORAD is a noncoding RNA that negatively regulates PUMILIO activity. The goal of this study was to determine the gene expression changes that result from knockout of NORAD or overexpression of PUMILIO and to test whether NORAD knockout causes PUMILIO hyperactivity. Methods: RNA-seq libraries were prepared using the TruSeq Stranded Total RNA with Ribo-Zero Human/Mouse/Rat Sample Preparation kit (Illumina) and sequenced using the 100 bp paired-end protocol on an Illumina HiSeq 2000. For comparing NORAD+/+ and NORAD-/- HCT116 cells, 3 biological replicates per genotype were sequenced. For PUM overexpression experiments, 3 replicates of GFP-expressing HCT116 cells (negative control) and 2 independent PUM1- or PUM2-overexpressing clones (2 replicates each) were sequenced. Results: Gene expression profiles show that PUMILIO target genes are downregulated in both NORAD knockout cells and PUMILIO overexpressing cells. Conclusions: These data indicate that NORAD sequesters PUMILIO, preventing excessive repression of PUMILIO target genes that are important for maintaining genomic stability. Overall design: Gene expression profiles of genetically modified HCT116 cells were determined by RNA-seq.","study_primary_id":"SRP066895"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066895","sample_accession":"SRS1186109","experiment_accession":"SRX1458632","run_accession":"SRR2969251","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Gene expression profiles in NORAD knockout and PUMILIO overexpressing cells","study_abstract":"Purpose: PUMILIO proteins are known to repress target genes by specifically binding to PUMILIO response elements (PREs) in target mRNAs. NORAD is a noncoding RNA that negatively regulates PUMILIO activity. The goal of this study was to determine the gene expression changes that result from knockout of NORAD or overexpression of PUMILIO and to test whether NORAD knockout causes PUMILIO hyperactivity. Methods: RNA-seq libraries were prepared using the TruSeq Stranded Total RNA with Ribo-Zero Human/Mouse/Rat Sample Preparation kit (Illumina) and sequenced using the 100 bp paired-end protocol on an Illumina HiSeq 2000. For comparing NORAD+/+ and NORAD-/- HCT116 cells, 3 biological replicates per genotype were sequenced. For PUM overexpression experiments, 3 replicates of GFP-expressing HCT116 cells (negative control) and 2 independent PUM1- or PUM2-overexpressing clones (2 replicates each) were sequenced. Results: Gene expression profiles show that PUMILIO target genes are downregulated in both NORAD knockout cells and PUMILIO overexpressing cells. Conclusions: These data indicate that NORAD sequesters PUMILIO, preventing excessive repression of PUMILIO target genes that are important for maintaining genomic stability. Overall design: Gene expression profiles of genetically modified HCT116 cells were determined by RNA-seq.","study_primary_id":"SRP066895"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066895","sample_accession":"SRS1186099","experiment_accession":"SRX1458640","run_accession":"SRR2969259","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Gene expression profiles in NORAD knockout and PUMILIO overexpressing cells","study_abstract":"Purpose: PUMILIO proteins are known to repress target genes by specifically binding to PUMILIO response elements (PREs) in target mRNAs. NORAD is a noncoding RNA that negatively regulates PUMILIO activity. The goal of this study was to determine the gene expression changes that result from knockout of NORAD or overexpression of PUMILIO and to test whether NORAD knockout causes PUMILIO hyperactivity. Methods: RNA-seq libraries were prepared using the TruSeq Stranded Total RNA with Ribo-Zero Human/Mouse/Rat Sample Preparation kit (Illumina) and sequenced using the 100 bp paired-end protocol on an Illumina HiSeq 2000. For comparing NORAD+/+ and NORAD-/- HCT116 cells, 3 biological replicates per genotype were sequenced. For PUM overexpression experiments, 3 replicates of GFP-expressing HCT116 cells (negative control) and 2 independent PUM1- or PUM2-overexpressing clones (2 replicates each) were sequenced. Results: Gene expression profiles show that PUMILIO target genes are downregulated in both NORAD knockout cells and PUMILIO overexpressing cells. Conclusions: These data indicate that NORAD sequesters PUMILIO, preventing excessive repression of PUMILIO target genes that are important for maintaining genomic stability. Overall design: Gene expression profiles of genetically modified HCT116 cells were determined by RNA-seq.","study_primary_id":"SRP066895"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066895","sample_accession":"SRS1186098","experiment_accession":"SRX1458641","run_accession":"SRR2969260","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Gene expression profiles in NORAD knockout and PUMILIO overexpressing cells","study_abstract":"Purpose: PUMILIO proteins are known to repress target genes by specifically binding to PUMILIO response elements (PREs) in target mRNAs. NORAD is a noncoding RNA that negatively regulates PUMILIO activity. The goal of this study was to determine the gene expression changes that result from knockout of NORAD or overexpression of PUMILIO and to test whether NORAD knockout causes PUMILIO hyperactivity. Methods: RNA-seq libraries were prepared using the TruSeq Stranded Total RNA with Ribo-Zero Human/Mouse/Rat Sample Preparation kit (Illumina) and sequenced using the 100 bp paired-end protocol on an Illumina HiSeq 2000. For comparing NORAD+/+ and NORAD-/- HCT116 cells, 3 biological replicates per genotype were sequenced. For PUM overexpression experiments, 3 replicates of GFP-expressing HCT116 cells (negative control) and 2 independent PUM1- or PUM2-overexpressing clones (2 replicates each) were sequenced. Results: Gene expression profiles show that PUMILIO target genes are downregulated in both NORAD knockout cells and PUMILIO overexpressing cells. Conclusions: These data indicate that NORAD sequesters PUMILIO, preventing excessive repression of PUMILIO target genes that are important for maintaining genomic stability. Overall design: Gene expression profiles of genetically modified HCT116 cells were determined by RNA-seq.","study_primary_id":"SRP066895"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066895","sample_accession":"SRS1186107","experiment_accession":"SRX1458634","run_accession":"SRR2969253","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Gene expression profiles in NORAD knockout and PUMILIO overexpressing cells","study_abstract":"Purpose: PUMILIO proteins are known to repress target genes by specifically binding to PUMILIO response elements (PREs) in target mRNAs. NORAD is a noncoding RNA that negatively regulates PUMILIO activity. The goal of this study was to determine the gene expression changes that result from knockout of NORAD or overexpression of PUMILIO and to test whether NORAD knockout causes PUMILIO hyperactivity. Methods: RNA-seq libraries were prepared using the TruSeq Stranded Total RNA with Ribo-Zero Human/Mouse/Rat Sample Preparation kit (Illumina) and sequenced using the 100 bp paired-end protocol on an Illumina HiSeq 2000. For comparing NORAD+/+ and NORAD-/- HCT116 cells, 3 biological replicates per genotype were sequenced. For PUM overexpression experiments, 3 replicates of GFP-expressing HCT116 cells (negative control) and 2 independent PUM1- or PUM2-overexpressing clones (2 replicates each) were sequenced. Results: Gene expression profiles show that PUMILIO target genes are downregulated in both NORAD knockout cells and PUMILIO overexpressing cells. Conclusions: These data indicate that NORAD sequesters PUMILIO, preventing excessive repression of PUMILIO target genes that are important for maintaining genomic stability. Overall design: Gene expression profiles of genetically modified HCT116 cells were determined by RNA-seq.","study_primary_id":"SRP066895"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189573","experiment_accession":"SRX1462151","run_accession":"SRR2972775","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189591","experiment_accession":"SRX1462133","run_accession":"SRR2972757","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189584","experiment_accession":"SRX1462140","run_accession":"SRR2972764","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189586","experiment_accession":"SRX1462138","run_accession":"SRR2972762","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189567","experiment_accession":"SRX1462157","run_accession":"SRR2972781","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189587","experiment_accession":"SRX1462137","run_accession":"SRR2972761","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189588","experiment_accession":"SRX1462136","run_accession":"SRR2972760","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189571","experiment_accession":"SRX1462153","run_accession":"SRR2972777","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189568","experiment_accession":"SRX1462156","run_accession":"SRR2972780","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189581","experiment_accession":"SRX1462143","run_accession":"SRR2972767","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189569","experiment_accession":"SRX1462155","run_accession":"SRR2972779","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189580","experiment_accession":"SRX1462144","run_accession":"SRR2972768","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189566","experiment_accession":"SRX1462158","run_accession":"SRR2972782","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189583","experiment_accession":"SRX1462141","run_accession":"SRR2972765","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189570","experiment_accession":"SRX1462154","run_accession":"SRR2972778","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189589","experiment_accession":"SRX1462135","run_accession":"SRR2972759","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189572","experiment_accession":"SRX1462152","run_accession":"SRR2972776","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189582","experiment_accession":"SRX1462142","run_accession":"SRR2972766","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189579","experiment_accession":"SRX1462145","run_accession":"SRR2972769","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189590","experiment_accession":"SRX1462134","run_accession":"SRR2972758","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP066967","sample_accession":"SRS1189585","experiment_accession":"SRX1462139","run_accession":"SRR2972763","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"Direct identification of hundreds of expression-modulating variants using a multiplexed reporter assay","study_abstract":"Although genetic studies have identified many hundreds of loci associated with human traits and diseases, pinpointing the causal alleles remains difficult, particularly for non-coding variants. To address this challenge, we have enhanced the sensitivity and reproducibility of the massively parallel reporter assay (MPRA), adapting it to identify variants that directly modulate gene expression. We then applied it to over 29,000 single nucleotide and insertion/deletion polymorphisms from 3,965 cis-expression quantitative trait loci (eQTL). We demonstrate strong correlation between our MPRA approach and existing measures of regulatory function, and determine an approximate sensitivity of ~20% with a positive predictive value of 60-65% to detect an eQTL causal allele. We identify 842 variants showing differential expression between alleles, including 53 well-annotated variants associated with diseases and traits. Thus, we have created a resource of concrete leads for understanding the genetic basis of specific phenotypes and illustrate the promise of this kind of approach for comprehensively interrogating how non-coding polymorphism shapes human biology. Overall design: The study consists of two separate MPRA experiments, a 78,958 oligo (79k study) and a 7,500 oligo library (7.5k). For each library we processed independent transfections into two lymphoblastoid cell lines; in total we completed 5 replicates of NA12878 and 3 replicates of NA19239. For the 79k library we also performed 5 replicate transfections into the hepatocarcinoma cell line HepG2. Raw data is provided as Illumina reads of the 20 bp barcode from the RNA extracted 24 hours post transfection as well as from the plasmid library used for transfection. We also provide oligo/barcode combinations from the ?gfp vector in the form of a tab delimited file containing the raw sequence reads of the barcode (column 1) and genomic sequence (column 2). Processed count files are unnormalized counts for each oligo acquired by summing all barcode matches together for each replicate.","study_primary_id":"SRP066967"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310678","experiment_accession":"SRX1600814","run_accession":"SRR3188099","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310696","experiment_accession":"SRX1600796","run_accession":"SRR3188081","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310673","experiment_accession":"SRX1600819","run_accession":"SRR3188104","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310684","experiment_accession":"SRX1600808","run_accession":"SRR3188093","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310677","experiment_accession":"SRX1600815","run_accession":"SRR3188100","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310694","experiment_accession":"SRX1600798","run_accession":"SRR3188083","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310674","experiment_accession":"SRX1600818","run_accession":"SRR3188103","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310692","experiment_accession":"SRX1600800","run_accession":"SRR3188085","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310698","experiment_accession":"SRX1600794","run_accession":"SRR3188079","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310693","experiment_accession":"SRX1600799","run_accession":"SRR3188084","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310679","experiment_accession":"SRX1600813","run_accession":"SRR3188098","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310683","experiment_accession":"SRX1600809","run_accession":"SRR3188094","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310697","experiment_accession":"SRX1600795","run_accession":"SRR3188080","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310686","experiment_accession":"SRX1600806","run_accession":"SRR3188091","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310688","experiment_accession":"SRX1600804","run_accession":"SRR3188089","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310689","experiment_accession":"SRX1600803","run_accession":"SRR3188088","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310672","experiment_accession":"SRX1600820","run_accession":"SRR3188105","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310691","experiment_accession":"SRX1600801","run_accession":"SRR3188086","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310690","experiment_accession":"SRX1600802","run_accession":"SRR3188087","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310685","experiment_accession":"SRX1600807","run_accession":"SRR3188092","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310675","experiment_accession":"SRX1600817","run_accession":"SRR3188102","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310681","experiment_accession":"SRX1600811","run_accession":"SRR3188096","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310682","experiment_accession":"SRX1600810","run_accession":"SRR3188095","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310687","experiment_accession":"SRX1600805","run_accession":"SRR3188090","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310695","experiment_accession":"SRX1600797","run_accession":"SRR3188082","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310680","experiment_accession":"SRX1600812","run_accession":"SRR3188097","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP070828","sample_accession":"SRS1310676","experiment_accession":"SRX1600816","run_accession":"SRR3188101","machine_type":"Illumina HiSeq 2500","paired_end":true,"study_title":"Identification Of Candidate Anti-Cancer Molecular Mechanisms Of Compound Kushen Injection Using Functional Genomics","study_abstract":"Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1.0 and 2.0 mg/mL), and 5-Fluorouracil (5-FU) was used to treat cells as a positive control. Cell proliferation and apoptosis activity were measured with XTT and Caspase-3 assays respectively. Transcriptome data of cells treated with CKI or 5-FU for 24 and 48 hours were acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment. Overall, we have comprehensively investigated the utility of transcriptome analysis with high-throughput sequencing to characterise the molecular response of cancer cells to a TCM drug, and provided a practical guideline for future molecular studies of TCM. Overall design: High-depth paired-end RNA-seq from MCF-7 cell line. Each sample contains 3 biological replicates.","study_primary_id":"SRP070828"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443766","experiment_accession":"SRX1771715","run_accession":"SRR3540234","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443759","experiment_accession":"SRX1771708","run_accession":"SRR3540227","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443749","experiment_accession":"SRX1771698","run_accession":"SRR3540217","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443753","experiment_accession":"SRX1771702","run_accession":"SRR3540221","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443764","experiment_accession":"SRX1771714","run_accession":"SRR3540233","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443757","experiment_accession":"SRX1771706","run_accession":"SRR3540225","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443763","experiment_accession":"SRX1771712","run_accession":"SRR3540231","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443767","experiment_accession":"SRX1771717","run_accession":"SRR3540236","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443768","experiment_accession":"SRX1771716","run_accession":"SRR3540235","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443762","experiment_accession":"SRX1771711","run_accession":"SRR3540230","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443752","experiment_accession":"SRX1771700","run_accession":"SRR3540219","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443765","experiment_accession":"SRX1771713","run_accession":"SRR3540232","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443761","experiment_accession":"SRX1771710","run_accession":"SRR3540229","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443755","experiment_accession":"SRX1771705","run_accession":"SRR3540224","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443756","experiment_accession":"SRX1771704","run_accession":"SRR3540223","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443751","experiment_accession":"SRX1771701","run_accession":"SRR3540220","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443760","experiment_accession":"SRX1771709","run_accession":"SRR3540228","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443758","experiment_accession":"SRX1771707","run_accession":"SRR3540226","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443750","experiment_accession":"SRX1771699","run_accession":"SRR3540218","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP075354","sample_accession":"SRS1443754","experiment_accession":"SRX1771703","run_accession":"SRR3540222","machine_type":"Illumina HiSeq 2000","paired_end":true,"study_title":"Transcriptome analysis of human cumulus cells reveals hypoxia as the main determinant of follicular senescence.","study_abstract":"RNA sequencing profiling of cumulus cells revealed that the follicles of older women have a compromised environment with hypoxic stress being the main contributor to age-related oocyte quality decay. Overall design: Twenty cumulus cells (CC) samples (from a total of 15 patients) were obtained from oocytes of either male factor or egg donor patients. RNA sequencing and bioinformatic tools were used to identify differentially expressed genes (DEGs) between CCs from seven aged and eight young patients (<35 (years old) y.o. vs >40 y.o.). Quantitative-PCR and immunoflourescent staining were used for validation.","study_primary_id":"SRP075354"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP077683","sample_accession":"SRS1533817","experiment_accession":"SRX1890832","run_accession":"SRR3735312","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"The effect of ADAM12 knockdown on gene expression in SUM159PT breast cancer cells","study_abstract":"The goal of the study was to assess a possible contribution of ADAM12 to the cancer stem cell phenotype of triple negative breast cancer cells. ADAM12 was knocked down in SUM159PT cells using a doxycycline-inducible shRNA system. shADAM12 or shControl cells were incubated with or without 1 µg/ml doxycycline for 4 days, followed by RNA sequencing.","study_primary_id":"SRP077683"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP077683","sample_accession":"SRS1533816","experiment_accession":"SRX1890831","run_accession":"SRR3735311","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"The effect of ADAM12 knockdown on gene expression in SUM159PT breast cancer cells","study_abstract":"The goal of the study was to assess a possible contribution of ADAM12 to the cancer stem cell phenotype of triple negative breast cancer cells. ADAM12 was knocked down in SUM159PT cells using a doxycycline-inducible shRNA system. shADAM12 or shControl cells were incubated with or without 1 µg/ml doxycycline for 4 days, followed by RNA sequencing.","study_primary_id":"SRP077683"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP077683","sample_accession":"SRS1533813","experiment_accession":"SRX1890828","run_accession":"SRR3735308","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"The effect of ADAM12 knockdown on gene expression in SUM159PT breast cancer cells","study_abstract":"The goal of the study was to assess a possible contribution of ADAM12 to the cancer stem cell phenotype of triple negative breast cancer cells. ADAM12 was knocked down in SUM159PT cells using a doxycycline-inducible shRNA system. shADAM12 or shControl cells were incubated with or without 1 µg/ml doxycycline for 4 days, followed by RNA sequencing.","study_primary_id":"SRP077683"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP077683","sample_accession":"SRS1533822","experiment_accession":"SRX1890837","run_accession":"SRR3735317","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"The effect of ADAM12 knockdown on gene expression in SUM159PT breast cancer cells","study_abstract":"The goal of the study was to assess a possible contribution of ADAM12 to the cancer stem cell phenotype of triple negative breast cancer cells. ADAM12 was knocked down in SUM159PT cells using a doxycycline-inducible shRNA system. shADAM12 or shControl cells were incubated with or without 1 µg/ml doxycycline for 4 days, followed by RNA sequencing.","study_primary_id":"SRP077683"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP077683","sample_accession":"SRS1533821","experiment_accession":"SRX1890836","run_accession":"SRR3735316","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"The effect of ADAM12 knockdown on gene expression in SUM159PT breast cancer cells","study_abstract":"The goal of the study was to assess a possible contribution of ADAM12 to the cancer stem cell phenotype of triple negative breast cancer cells. ADAM12 was knocked down in SUM159PT cells using a doxycycline-inducible shRNA system. shADAM12 or shControl cells were incubated with or without 1 µg/ml doxycycline for 4 days, followed by RNA sequencing.","study_primary_id":"SRP077683"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP077683","sample_accession":"SRS1533814","experiment_accession":"SRX1890829","run_accession":"SRR3735309","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"The effect of ADAM12 knockdown on gene expression in SUM159PT breast cancer cells","study_abstract":"The goal of the study was to assess a possible contribution of ADAM12 to the cancer stem cell phenotype of triple negative breast cancer cells. ADAM12 was knocked down in SUM159PT cells using a doxycycline-inducible shRNA system. shADAM12 or shControl cells were incubated with or without 1 µg/ml doxycycline for 4 days, followed by RNA sequencing.","study_primary_id":"SRP077683"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP077683","sample_accession":"SRS1533815","experiment_accession":"SRX1890830","run_accession":"SRR3735310","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"The effect of ADAM12 knockdown on gene expression in SUM159PT breast cancer cells","study_abstract":"The goal of the study was to assess a possible contribution of ADAM12 to the cancer stem cell phenotype of triple negative breast cancer cells. ADAM12 was knocked down in SUM159PT cells using a doxycycline-inducible shRNA system. shADAM12 or shControl cells were incubated with or without 1 µg/ml doxycycline for 4 days, followed by RNA sequencing.","study_primary_id":"SRP077683"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP077683","sample_accession":"SRS1533820","experiment_accession":"SRX1890835","run_accession":"SRR3735315","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"The effect of ADAM12 knockdown on gene expression in SUM159PT breast cancer cells","study_abstract":"The goal of the study was to assess a possible contribution of ADAM12 to the cancer stem cell phenotype of triple negative breast cancer cells. ADAM12 was knocked down in SUM159PT cells using a doxycycline-inducible shRNA system. shADAM12 or shControl cells were incubated with or without 1 µg/ml doxycycline for 4 days, followed by RNA sequencing.","study_primary_id":"SRP077683"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP077683","sample_accession":"SRS1533819","experiment_accession":"SRX1890834","run_accession":"SRR3735314","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"The effect of ADAM12 knockdown on gene expression in SUM159PT breast cancer cells","study_abstract":"The goal of the study was to assess a possible contribution of ADAM12 to the cancer stem cell phenotype of triple negative breast cancer cells. ADAM12 was knocked down in SUM159PT cells using a doxycycline-inducible shRNA system. shADAM12 or shControl cells were incubated with or without 1 µg/ml doxycycline for 4 days, followed by RNA sequencing.","study_primary_id":"SRP077683"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP077683","sample_accession":"SRS1533823","experiment_accession":"SRX1890838","run_accession":"SRR3735318","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"The effect of ADAM12 knockdown on gene expression in SUM159PT breast cancer cells","study_abstract":"The goal of the study was to assess a possible contribution of ADAM12 to the cancer stem cell phenotype of triple negative breast cancer cells. ADAM12 was knocked down in SUM159PT cells using a doxycycline-inducible shRNA system. shADAM12 or shControl cells were incubated with or without 1 µg/ml doxycycline for 4 days, followed by RNA sequencing.","study_primary_id":"SRP077683"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP077683","sample_accession":"SRS1533818","experiment_accession":"SRX1890833","run_accession":"SRR3735313","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"The effect of ADAM12 knockdown on gene expression in SUM159PT breast cancer cells","study_abstract":"The goal of the study was to assess a possible contribution of ADAM12 to the cancer stem cell phenotype of triple negative breast cancer cells. ADAM12 was knocked down in SUM159PT cells using a doxycycline-inducible shRNA system. shADAM12 or shControl cells were incubated with or without 1 µg/ml doxycycline for 4 days, followed by RNA sequencing.","study_primary_id":"SRP077683"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP077683","sample_accession":"SRS1533812","experiment_accession":"SRX1890827","run_accession":"SRR3735306","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"The effect of ADAM12 knockdown on gene expression in SUM159PT breast cancer cells","study_abstract":"The goal of the study was to assess a possible contribution of ADAM12 to the cancer stem cell phenotype of triple negative breast cancer cells. ADAM12 was knocked down in SUM159PT cells using a doxycycline-inducible shRNA system. shADAM12 or shControl cells were incubated with or without 1 µg/ml doxycycline for 4 days, followed by RNA sequencing.","study_primary_id":"SRP077683"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963388","experiment_accession":"SRX2544429","run_accession":"SRR5237376","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963388","experiment_accession":"SRX2544429","run_accession":"SRR5237377","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963388","experiment_accession":"SRX2544429","run_accession":"SRR5237378","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963385","experiment_accession":"SRX2544426","run_accession":"SRR5237367","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963385","experiment_accession":"SRX2544426","run_accession":"SRR5237368","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963385","experiment_accession":"SRX2544426","run_accession":"SRR5237369","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963389","experiment_accession":"SRX2544430","run_accession":"SRR5237379","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963389","experiment_accession":"SRX2544430","run_accession":"SRR5237380","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963389","experiment_accession":"SRX2544430","run_accession":"SRR5237381","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963387","experiment_accession":"SRX2544428","run_accession":"SRR5237373","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963387","experiment_accession":"SRX2544428","run_accession":"SRR5237374","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963387","experiment_accession":"SRX2544428","run_accession":"SRR5237375","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963378","experiment_accession":"SRX2544419","run_accession":"SRR5237346","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963378","experiment_accession":"SRX2544419","run_accession":"SRR5237347","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963378","experiment_accession":"SRX2544419","run_accession":"SRR5237348","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963380","experiment_accession":"SRX2544421","run_accession":"SRR5237352","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963380","experiment_accession":"SRX2544421","run_accession":"SRR5237353","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963380","experiment_accession":"SRX2544421","run_accession":"SRR5237354","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963383","experiment_accession":"SRX2544424","run_accession":"SRR5237361","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963383","experiment_accession":"SRX2544424","run_accession":"SRR5237362","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963383","experiment_accession":"SRX2544424","run_accession":"SRR5237363","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963386","experiment_accession":"SRX2544427","run_accession":"SRR5237370","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963386","experiment_accession":"SRX2544427","run_accession":"SRR5237371","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963386","experiment_accession":"SRX2544427","run_accession":"SRR5237372","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963382","experiment_accession":"SRX2544423","run_accession":"SRR5237358","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963382","experiment_accession":"SRX2544423","run_accession":"SRR5237359","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963382","experiment_accession":"SRX2544423","run_accession":"SRR5237360","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963384","experiment_accession":"SRX2544425","run_accession":"SRR5237364","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963384","experiment_accession":"SRX2544425","run_accession":"SRR5237365","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963384","experiment_accession":"SRX2544425","run_accession":"SRR5237366","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963379","experiment_accession":"SRX2544420","run_accession":"SRR5237349","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963379","experiment_accession":"SRX2544420","run_accession":"SRR5237350","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963379","experiment_accession":"SRX2544420","run_accession":"SRR5237351","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963381","experiment_accession":"SRX2544422","run_accession":"SRR5237355","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963381","experiment_accession":"SRX2544422","run_accession":"SRR5237356","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP099048","sample_accession":"SRS1963381","experiment_accession":"SRX2544422","run_accession":"SRR5237357","machine_type":"AB 5500xl Genetic Analyzer","paired_end":true,"study_title":"RNASeq of juvenile keratinocytes, melanocytes, fibroblasts and whole skin","study_abstract":"We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties. Overall design: From each of the healthy juvnile skin tissue samples a whole skin sample was taken and three skin cell types (keratinocytes, melanocytes and fibroblasts) were harvested and cultivated. We chose 12 total RNA samples, extracted from 4 keratinocytes (Kc), 4 melanocytes (Mc), 2 fibroblasts (FB) and 2 whole skin samples for library preparation.","study_primary_id":"SRP099048"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP102520","sample_accession":"SRS2074153","experiment_accession":"SRX2675027","run_accession":"SRR5379795","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"R-ChIP Using Inactive RNase H Reveals Dynamic Coupling of R-loops with Transcriptional Pausing at Gene Promoters","study_abstract":"R-loop, a three-stranded RNA/DNA structure, has been linked to induced genome instability and regulated gene expression. To enable precision analysis of R-loops in vivo, we develop an RNase H-based approach, revealing predominant R-loop formation near gene promoters with strong G/C skew and propensity to form G-quadruplex in non-template DNA, corroborating with all biochemically established properties of R-loops. Transcription perturbation experiments further indicate that R-loop induction correlates to transcriptional pausing. Interestingly, we note that most mapped R-loops are each linked to a nearby free RNA end, and by using a ribozyme to co-transcriptionally cleave nascent RNA, we demonstrate that such free RNA end coupled with a G/C-skewed sequence is necessary and sufficient to induce R-loop. These findings provide a topological solution for RNA invasion into duplex DNA and suggest an order for R-loop initiation and elongation in an opposite direction to that previously proposed. Overall design: We initially developped our R-ChIP technology in HEK293 cells to characterize the genome-wide in vivo R-loops, and also applied it on K562 cell to compare with existing R-loop detection methods. Furthermore, to examine the functional interplay between R-loop and RNAPII pausing and pause release at promoter region, we generated two sets of biologically replicated R-ChIP libraries, each set on mock-treated HEK293T cells [DRB(-)] or cells treated with DRB for 2 hrs [DRB(+)] or after DRB removal for 30 min [post-DRB]. We also performed GRO-seq to monitor transcriptionally engaged RNAPII under these conditions. All R-ChIP data have two to three replicates and controls, and GRO-seq data have two replicates.","study_primary_id":"SRP102520"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP102520","sample_accession":"SRS2074149","experiment_accession":"SRX2675023","run_accession":"SRR5379791","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"R-ChIP Using Inactive RNase H Reveals Dynamic Coupling of R-loops with Transcriptional Pausing at Gene Promoters","study_abstract":"R-loop, a three-stranded RNA/DNA structure, has been linked to induced genome instability and regulated gene expression. To enable precision analysis of R-loops in vivo, we develop an RNase H-based approach, revealing predominant R-loop formation near gene promoters with strong G/C skew and propensity to form G-quadruplex in non-template DNA, corroborating with all biochemically established properties of R-loops. Transcription perturbation experiments further indicate that R-loop induction correlates to transcriptional pausing. Interestingly, we note that most mapped R-loops are each linked to a nearby free RNA end, and by using a ribozyme to co-transcriptionally cleave nascent RNA, we demonstrate that such free RNA end coupled with a G/C-skewed sequence is necessary and sufficient to induce R-loop. These findings provide a topological solution for RNA invasion into duplex DNA and suggest an order for R-loop initiation and elongation in an opposite direction to that previously proposed. Overall design: We initially developped our R-ChIP technology in HEK293 cells to characterize the genome-wide in vivo R-loops, and also applied it on K562 cell to compare with existing R-loop detection methods. Furthermore, to examine the functional interplay between R-loop and RNAPII pausing and pause release at promoter region, we generated two sets of biologically replicated R-ChIP libraries, each set on mock-treated HEK293T cells [DRB(-)] or cells treated with DRB for 2 hrs [DRB(+)] or after DRB removal for 30 min [post-DRB]. We also performed GRO-seq to monitor transcriptionally engaged RNAPII under these conditions. All R-ChIP data have two to three replicates and controls, and GRO-seq data have two replicates.","study_primary_id":"SRP102520"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP102520","sample_accession":"SRS2074150","experiment_accession":"SRX2675024","run_accession":"SRR5379792","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"R-ChIP Using Inactive RNase H Reveals Dynamic Coupling of R-loops with Transcriptional Pausing at Gene Promoters","study_abstract":"R-loop, a three-stranded RNA/DNA structure, has been linked to induced genome instability and regulated gene expression. To enable precision analysis of R-loops in vivo, we develop an RNase H-based approach, revealing predominant R-loop formation near gene promoters with strong G/C skew and propensity to form G-quadruplex in non-template DNA, corroborating with all biochemically established properties of R-loops. Transcription perturbation experiments further indicate that R-loop induction correlates to transcriptional pausing. Interestingly, we note that most mapped R-loops are each linked to a nearby free RNA end, and by using a ribozyme to co-transcriptionally cleave nascent RNA, we demonstrate that such free RNA end coupled with a G/C-skewed sequence is necessary and sufficient to induce R-loop. These findings provide a topological solution for RNA invasion into duplex DNA and suggest an order for R-loop initiation and elongation in an opposite direction to that previously proposed. Overall design: We initially developped our R-ChIP technology in HEK293 cells to characterize the genome-wide in vivo R-loops, and also applied it on K562 cell to compare with existing R-loop detection methods. Furthermore, to examine the functional interplay between R-loop and RNAPII pausing and pause release at promoter region, we generated two sets of biologically replicated R-ChIP libraries, each set on mock-treated HEK293T cells [DRB(-)] or cells treated with DRB for 2 hrs [DRB(+)] or after DRB removal for 30 min [post-DRB]. We also performed GRO-seq to monitor transcriptionally engaged RNAPII under these conditions. All R-ChIP data have two to three replicates and controls, and GRO-seq data have two replicates.","study_primary_id":"SRP102520"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP102520","sample_accession":"SRS2074151","experiment_accession":"SRX2675026","run_accession":"SRR5379794","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"R-ChIP Using Inactive RNase H Reveals Dynamic Coupling of R-loops with Transcriptional Pausing at Gene Promoters","study_abstract":"R-loop, a three-stranded RNA/DNA structure, has been linked to induced genome instability and regulated gene expression. To enable precision analysis of R-loops in vivo, we develop an RNase H-based approach, revealing predominant R-loop formation near gene promoters with strong G/C skew and propensity to form G-quadruplex in non-template DNA, corroborating with all biochemically established properties of R-loops. Transcription perturbation experiments further indicate that R-loop induction correlates to transcriptional pausing. Interestingly, we note that most mapped R-loops are each linked to a nearby free RNA end, and by using a ribozyme to co-transcriptionally cleave nascent RNA, we demonstrate that such free RNA end coupled with a G/C-skewed sequence is necessary and sufficient to induce R-loop. These findings provide a topological solution for RNA invasion into duplex DNA and suggest an order for R-loop initiation and elongation in an opposite direction to that previously proposed. Overall design: We initially developped our R-ChIP technology in HEK293 cells to characterize the genome-wide in vivo R-loops, and also applied it on K562 cell to compare with existing R-loop detection methods. Furthermore, to examine the functional interplay between R-loop and RNAPII pausing and pause release at promoter region, we generated two sets of biologically replicated R-ChIP libraries, each set on mock-treated HEK293T cells [DRB(-)] or cells treated with DRB for 2 hrs [DRB(+)] or after DRB removal for 30 min [post-DRB]. We also performed GRO-seq to monitor transcriptionally engaged RNAPII under these conditions. All R-ChIP data have two to three replicates and controls, and GRO-seq data have two replicates.","study_primary_id":"SRP102520"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP102520","sample_accession":"SRS2074152","experiment_accession":"SRX2675025","run_accession":"SRR5379793","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"R-ChIP Using Inactive RNase H Reveals Dynamic Coupling of R-loops with Transcriptional Pausing at Gene Promoters","study_abstract":"R-loop, a three-stranded RNA/DNA structure, has been linked to induced genome instability and regulated gene expression. To enable precision analysis of R-loops in vivo, we develop an RNase H-based approach, revealing predominant R-loop formation near gene promoters with strong G/C skew and propensity to form G-quadruplex in non-template DNA, corroborating with all biochemically established properties of R-loops. Transcription perturbation experiments further indicate that R-loop induction correlates to transcriptional pausing. Interestingly, we note that most mapped R-loops are each linked to a nearby free RNA end, and by using a ribozyme to co-transcriptionally cleave nascent RNA, we demonstrate that such free RNA end coupled with a G/C-skewed sequence is necessary and sufficient to induce R-loop. These findings provide a topological solution for RNA invasion into duplex DNA and suggest an order for R-loop initiation and elongation in an opposite direction to that previously proposed. Overall design: We initially developped our R-ChIP technology in HEK293 cells to characterize the genome-wide in vivo R-loops, and also applied it on K562 cell to compare with existing R-loop detection methods. Furthermore, to examine the functional interplay between R-loop and RNAPII pausing and pause release at promoter region, we generated two sets of biologically replicated R-ChIP libraries, each set on mock-treated HEK293T cells [DRB(-)] or cells treated with DRB for 2 hrs [DRB(+)] or after DRB removal for 30 min [post-DRB]. We also performed GRO-seq to monitor transcriptionally engaged RNAPII under these conditions. All R-ChIP data have two to three replicates and controls, and GRO-seq data have two replicates.","study_primary_id":"SRP102520"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP102520","sample_accession":"SRS2074148","experiment_accession":"SRX2675022","run_accession":"SRR5379790","machine_type":"Illumina HiSeq 2500","paired_end":false,"study_title":"R-ChIP Using Inactive RNase H Reveals Dynamic Coupling of R-loops with Transcriptional Pausing at Gene Promoters","study_abstract":"R-loop, a three-stranded RNA/DNA structure, has been linked to induced genome instability and regulated gene expression. To enable precision analysis of R-loops in vivo, we develop an RNase H-based approach, revealing predominant R-loop formation near gene promoters with strong G/C skew and propensity to form G-quadruplex in non-template DNA, corroborating with all biochemically established properties of R-loops. Transcription perturbation experiments further indicate that R-loop induction correlates to transcriptional pausing. Interestingly, we note that most mapped R-loops are each linked to a nearby free RNA end, and by using a ribozyme to co-transcriptionally cleave nascent RNA, we demonstrate that such free RNA end coupled with a G/C-skewed sequence is necessary and sufficient to induce R-loop. These findings provide a topological solution for RNA invasion into duplex DNA and suggest an order for R-loop initiation and elongation in an opposite direction to that previously proposed. Overall design: We initially developped our R-ChIP technology in HEK293 cells to characterize the genome-wide in vivo R-loops, and also applied it on K562 cell to compare with existing R-loop detection methods. Furthermore, to examine the functional interplay between R-loop and RNAPII pausing and pause release at promoter region, we generated two sets of biologically replicated R-ChIP libraries, each set on mock-treated HEK293T cells [DRB(-)] or cells treated with DRB for 2 hrs [DRB(+)] or after DRB removal for 30 min [post-DRB]. We also performed GRO-seq to monitor transcriptionally engaged RNAPII under these conditions. All R-ChIP data have two to three replicates and controls, and GRO-seq data have two replicates.","study_primary_id":"SRP102520"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP110569","sample_accession":"SRS2316439","experiment_accession":"SRX2959427","run_accession":"SRR5759600","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Human RNase L Employs a Signaling Mechanism to Arrest Translation","study_abstract":"To identify small RNA cleaved by RNaseL, we captured intracellular RNA with 2''-3'' cyclic phosphates by ligation an Illumina-compatible adaptor and the RNA ligase RtcB. Overall design: Small RNAs with 2''-3'' cyclic phosphate were ligated to an adaptor with RtcB and converted to Illumina small RNA sequencing libraries. Three independent methods were used to activate RNase L: transfection of poly-IC, a synthetic dsRNA, semi-permeabilization of cells in the presence of 2-5A, and overexpression of RNase L. We also examined basal activity of RNase L by 2''-3'' cyclic phosphate small RNA in WT and RNase L knockout Hap1 cells. Additionally, we showed that the Ire1, an RNase L homologue, does not cleave small RNAs. Last, we show that A549 do not show mRNA decay after prolonged treatment with 2-5A.","study_primary_id":"SRP110569"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP110569","sample_accession":"SRS2316433","experiment_accession":"SRX2959421","run_accession":"SRR5759594","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Human RNase L Employs a Signaling Mechanism to Arrest Translation","study_abstract":"To identify small RNA cleaved by RNaseL, we captured intracellular RNA with 2''-3'' cyclic phosphates by ligation an Illumina-compatible adaptor and the RNA ligase RtcB. Overall design: Small RNAs with 2''-3'' cyclic phosphate were ligated to an adaptor with RtcB and converted to Illumina small RNA sequencing libraries. Three independent methods were used to activate RNase L: transfection of poly-IC, a synthetic dsRNA, semi-permeabilization of cells in the presence of 2-5A, and overexpression of RNase L. We also examined basal activity of RNase L by 2''-3'' cyclic phosphate small RNA in WT and RNase L knockout Hap1 cells. Additionally, we showed that the Ire1, an RNase L homologue, does not cleave small RNAs. Last, we show that A549 do not show mRNA decay after prolonged treatment with 2-5A.","study_primary_id":"SRP110569"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP110569","sample_accession":"SRS2316440","experiment_accession":"SRX2959428","run_accession":"SRR5759601","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Human RNase L Employs a Signaling Mechanism to Arrest Translation","study_abstract":"To identify small RNA cleaved by RNaseL, we captured intracellular RNA with 2''-3'' cyclic phosphates by ligation an Illumina-compatible adaptor and the RNA ligase RtcB. Overall design: Small RNAs with 2''-3'' cyclic phosphate were ligated to an adaptor with RtcB and converted to Illumina small RNA sequencing libraries. Three independent methods were used to activate RNase L: transfection of poly-IC, a synthetic dsRNA, semi-permeabilization of cells in the presence of 2-5A, and overexpression of RNase L. We also examined basal activity of RNase L by 2''-3'' cyclic phosphate small RNA in WT and RNase L knockout Hap1 cells. Additionally, we showed that the Ire1, an RNase L homologue, does not cleave small RNAs. Last, we show that A549 do not show mRNA decay after prolonged treatment with 2-5A.","study_primary_id":"SRP110569"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP110569","sample_accession":"SRS2316442","experiment_accession":"SRX2959430","run_accession":"SRR5759603","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Human RNase L Employs a Signaling Mechanism to Arrest Translation","study_abstract":"To identify small RNA cleaved by RNaseL, we captured intracellular RNA with 2''-3'' cyclic phosphates by ligation an Illumina-compatible adaptor and the RNA ligase RtcB. Overall design: Small RNAs with 2''-3'' cyclic phosphate were ligated to an adaptor with RtcB and converted to Illumina small RNA sequencing libraries. Three independent methods were used to activate RNase L: transfection of poly-IC, a synthetic dsRNA, semi-permeabilization of cells in the presence of 2-5A, and overexpression of RNase L. We also examined basal activity of RNase L by 2''-3'' cyclic phosphate small RNA in WT and RNase L knockout Hap1 cells. Additionally, we showed that the Ire1, an RNase L homologue, does not cleave small RNAs. Last, we show that A549 do not show mRNA decay after prolonged treatment with 2-5A.","study_primary_id":"SRP110569"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP110569","sample_accession":"SRS2316441","experiment_accession":"SRX2959429","run_accession":"SRR5759602","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Human RNase L Employs a Signaling Mechanism to Arrest Translation","study_abstract":"To identify small RNA cleaved by RNaseL, we captured intracellular RNA with 2''-3'' cyclic phosphates by ligation an Illumina-compatible adaptor and the RNA ligase RtcB. Overall design: Small RNAs with 2''-3'' cyclic phosphate were ligated to an adaptor with RtcB and converted to Illumina small RNA sequencing libraries. Three independent methods were used to activate RNase L: transfection of poly-IC, a synthetic dsRNA, semi-permeabilization of cells in the presence of 2-5A, and overexpression of RNase L. We also examined basal activity of RNase L by 2''-3'' cyclic phosphate small RNA in WT and RNase L knockout Hap1 cells. Additionally, we showed that the Ire1, an RNase L homologue, does not cleave small RNAs. Last, we show that A549 do not show mRNA decay after prolonged treatment with 2-5A.","study_primary_id":"SRP110569"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP110569","sample_accession":"SRS2316430","experiment_accession":"SRX2959418","run_accession":"SRR5759591","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Human RNase L Employs a Signaling Mechanism to Arrest Translation","study_abstract":"To identify small RNA cleaved by RNaseL, we captured intracellular RNA with 2''-3'' cyclic phosphates by ligation an Illumina-compatible adaptor and the RNA ligase RtcB. Overall design: Small RNAs with 2''-3'' cyclic phosphate were ligated to an adaptor with RtcB and converted to Illumina small RNA sequencing libraries. Three independent methods were used to activate RNase L: transfection of poly-IC, a synthetic dsRNA, semi-permeabilization of cells in the presence of 2-5A, and overexpression of RNase L. We also examined basal activity of RNase L by 2''-3'' cyclic phosphate small RNA in WT and RNase L knockout Hap1 cells. Additionally, we showed that the Ire1, an RNase L homologue, does not cleave small RNAs. Last, we show that A549 do not show mRNA decay after prolonged treatment with 2-5A.","study_primary_id":"SRP110569"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP110569","sample_accession":"SRS2316431","experiment_accession":"SRX2959419","run_accession":"SRR5759592","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Human RNase L Employs a Signaling Mechanism to Arrest Translation","study_abstract":"To identify small RNA cleaved by RNaseL, we captured intracellular RNA with 2''-3'' cyclic phosphates by ligation an Illumina-compatible adaptor and the RNA ligase RtcB. Overall design: Small RNAs with 2''-3'' cyclic phosphate were ligated to an adaptor with RtcB and converted to Illumina small RNA sequencing libraries. Three independent methods were used to activate RNase L: transfection of poly-IC, a synthetic dsRNA, semi-permeabilization of cells in the presence of 2-5A, and overexpression of RNase L. We also examined basal activity of RNase L by 2''-3'' cyclic phosphate small RNA in WT and RNase L knockout Hap1 cells. Additionally, we showed that the Ire1, an RNase L homologue, does not cleave small RNAs. Last, we show that A549 do not show mRNA decay after prolonged treatment with 2-5A.","study_primary_id":"SRP110569"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP110569","sample_accession":"SRS2316438","experiment_accession":"SRX2959426","run_accession":"SRR5759599","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Human RNase L Employs a Signaling Mechanism to Arrest Translation","study_abstract":"To identify small RNA cleaved by RNaseL, we captured intracellular RNA with 2''-3'' cyclic phosphates by ligation an Illumina-compatible adaptor and the RNA ligase RtcB. Overall design: Small RNAs with 2''-3'' cyclic phosphate were ligated to an adaptor with RtcB and converted to Illumina small RNA sequencing libraries. Three independent methods were used to activate RNase L: transfection of poly-IC, a synthetic dsRNA, semi-permeabilization of cells in the presence of 2-5A, and overexpression of RNase L. We also examined basal activity of RNase L by 2''-3'' cyclic phosphate small RNA in WT and RNase L knockout Hap1 cells. Additionally, we showed that the Ire1, an RNase L homologue, does not cleave small RNAs. Last, we show that A549 do not show mRNA decay after prolonged treatment with 2-5A.","study_primary_id":"SRP110569"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP110569","sample_accession":"SRS2316437","experiment_accession":"SRX2959425","run_accession":"SRR5759598","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Human RNase L Employs a Signaling Mechanism to Arrest Translation","study_abstract":"To identify small RNA cleaved by RNaseL, we captured intracellular RNA with 2''-3'' cyclic phosphates by ligation an Illumina-compatible adaptor and the RNA ligase RtcB. Overall design: Small RNAs with 2''-3'' cyclic phosphate were ligated to an adaptor with RtcB and converted to Illumina small RNA sequencing libraries. Three independent methods were used to activate RNase L: transfection of poly-IC, a synthetic dsRNA, semi-permeabilization of cells in the presence of 2-5A, and overexpression of RNase L. We also examined basal activity of RNase L by 2''-3'' cyclic phosphate small RNA in WT and RNase L knockout Hap1 cells. Additionally, we showed that the Ire1, an RNase L homologue, does not cleave small RNAs. Last, we show that A549 do not show mRNA decay after prolonged treatment with 2-5A.","study_primary_id":"SRP110569"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP110569","sample_accession":"SRS2316432","experiment_accession":"SRX2959420","run_accession":"SRR5759593","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Human RNase L Employs a Signaling Mechanism to Arrest Translation","study_abstract":"To identify small RNA cleaved by RNaseL, we captured intracellular RNA with 2''-3'' cyclic phosphates by ligation an Illumina-compatible adaptor and the RNA ligase RtcB. Overall design: Small RNAs with 2''-3'' cyclic phosphate were ligated to an adaptor with RtcB and converted to Illumina small RNA sequencing libraries. Three independent methods were used to activate RNase L: transfection of poly-IC, a synthetic dsRNA, semi-permeabilization of cells in the presence of 2-5A, and overexpression of RNase L. We also examined basal activity of RNase L by 2''-3'' cyclic phosphate small RNA in WT and RNase L knockout Hap1 cells. Additionally, we showed that the Ire1, an RNase L homologue, does not cleave small RNAs. Last, we show that A549 do not show mRNA decay after prolonged treatment with 2-5A.","study_primary_id":"SRP110569"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP110569","sample_accession":"SRS2316435","experiment_accession":"SRX2959423","run_accession":"SRR5759596","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Human RNase L Employs a Signaling Mechanism to Arrest Translation","study_abstract":"To identify small RNA cleaved by RNaseL, we captured intracellular RNA with 2''-3'' cyclic phosphates by ligation an Illumina-compatible adaptor and the RNA ligase RtcB. Overall design: Small RNAs with 2''-3'' cyclic phosphate were ligated to an adaptor with RtcB and converted to Illumina small RNA sequencing libraries. Three independent methods were used to activate RNase L: transfection of poly-IC, a synthetic dsRNA, semi-permeabilization of cells in the presence of 2-5A, and overexpression of RNase L. We also examined basal activity of RNase L by 2''-3'' cyclic phosphate small RNA in WT and RNase L knockout Hap1 cells. Additionally, we showed that the Ire1, an RNase L homologue, does not cleave small RNAs. Last, we show that A549 do not show mRNA decay after prolonged treatment with 2-5A.","study_primary_id":"SRP110569"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP110569","sample_accession":"SRS2316436","experiment_accession":"SRX2959424","run_accession":"SRR5759597","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Human RNase L Employs a Signaling Mechanism to Arrest Translation","study_abstract":"To identify small RNA cleaved by RNaseL, we captured intracellular RNA with 2''-3'' cyclic phosphates by ligation an Illumina-compatible adaptor and the RNA ligase RtcB. Overall design: Small RNAs with 2''-3'' cyclic phosphate were ligated to an adaptor with RtcB and converted to Illumina small RNA sequencing libraries. Three independent methods were used to activate RNase L: transfection of poly-IC, a synthetic dsRNA, semi-permeabilization of cells in the presence of 2-5A, and overexpression of RNase L. We also examined basal activity of RNase L by 2''-3'' cyclic phosphate small RNA in WT and RNase L knockout Hap1 cells. Additionally, we showed that the Ire1, an RNase L homologue, does not cleave small RNAs. Last, we show that A549 do not show mRNA decay after prolonged treatment with 2-5A.","study_primary_id":"SRP110569"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP110569","sample_accession":"SRS2316434","experiment_accession":"SRX2959422","run_accession":"SRR5759595","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Human RNase L Employs a Signaling Mechanism to Arrest Translation","study_abstract":"To identify small RNA cleaved by RNaseL, we captured intracellular RNA with 2''-3'' cyclic phosphates by ligation an Illumina-compatible adaptor and the RNA ligase RtcB. Overall design: Small RNAs with 2''-3'' cyclic phosphate were ligated to an adaptor with RtcB and converted to Illumina small RNA sequencing libraries. Three independent methods were used to activate RNase L: transfection of poly-IC, a synthetic dsRNA, semi-permeabilization of cells in the presence of 2-5A, and overexpression of RNase L. We also examined basal activity of RNase L by 2''-3'' cyclic phosphate small RNA in WT and RNase L knockout Hap1 cells. Additionally, we showed that the Ire1, an RNase L homologue, does not cleave small RNAs. Last, we show that A549 do not show mRNA decay after prolonged treatment with 2-5A.","study_primary_id":"SRP110569"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP110569","sample_accession":"SRS2316429","experiment_accession":"SRX2959417","run_accession":"SRR5759590","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Human RNase L Employs a Signaling Mechanism to Arrest Translation","study_abstract":"To identify small RNA cleaved by RNaseL, we captured intracellular RNA with 2''-3'' cyclic phosphates by ligation an Illumina-compatible adaptor and the RNA ligase RtcB. Overall design: Small RNAs with 2''-3'' cyclic phosphate were ligated to an adaptor with RtcB and converted to Illumina small RNA sequencing libraries. Three independent methods were used to activate RNase L: transfection of poly-IC, a synthetic dsRNA, semi-permeabilization of cells in the presence of 2-5A, and overexpression of RNase L. We also examined basal activity of RNase L by 2''-3'' cyclic phosphate small RNA in WT and RNase L knockout Hap1 cells. Additionally, we showed that the Ire1, an RNase L homologue, does not cleave small RNAs. Last, we show that A549 do not show mRNA decay after prolonged treatment with 2-5A.","study_primary_id":"SRP110569"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP110569","sample_accession":"SRS2316443","experiment_accession":"SRX2959431","run_accession":"SRR5759604","machine_type":"Illumina HiSeq 2000","paired_end":false,"study_title":"Human RNase L Employs a Signaling Mechanism to Arrest Translation","study_abstract":"To identify small RNA cleaved by RNaseL, we captured intracellular RNA with 2''-3'' cyclic phosphates by ligation an Illumina-compatible adaptor and the RNA ligase RtcB. Overall design: Small RNAs with 2''-3'' cyclic phosphate were ligated to an adaptor with RtcB and converted to Illumina small RNA sequencing libraries. Three independent methods were used to activate RNase L: transfection of poly-IC, a synthetic dsRNA, semi-permeabilization of cells in the presence of 2-5A, and overexpression of RNase L. We also examined basal activity of RNase L by 2''-3'' cyclic phosphate small RNA in WT and RNase L knockout Hap1 cells. Additionally, we showed that the Ire1, an RNase L homologue, does not cleave small RNAs. Last, we show that A549 do not show mRNA decay after prolonged treatment with 2-5A.","study_primary_id":"SRP110569"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP111405","sample_accession":"SRS2344233","experiment_accession":"SRX2992278","run_accession":"SRR5813786","machine_type":"NextSeq 500","paired_end":true,"study_title":"IFNa impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing","study_abstract":"IFN-a impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing.","study_primary_id":"SRP111405"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP111405","sample_accession":"SRS2344233","experiment_accession":"SRX2992282","run_accession":"SRR5813782","machine_type":"NextSeq 500","paired_end":true,"study_title":"IFNa impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing","study_abstract":"IFN-a impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing.","study_primary_id":"SRP111405"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP111405","sample_accession":"SRS2344233","experiment_accession":"SRX2992284","run_accession":"SRR5813780","machine_type":"NextSeq 500","paired_end":true,"study_title":"IFNa impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing","study_abstract":"IFN-a impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing.","study_primary_id":"SRP111405"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP111405","sample_accession":"SRS2344233","experiment_accession":"SRX2992279","run_accession":"SRR5813785","machine_type":"NextSeq 500","paired_end":true,"study_title":"IFNa impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing","study_abstract":"IFN-a impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing.","study_primary_id":"SRP111405"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP111405","sample_accession":"SRS2344233","experiment_accession":"SRX2992280","run_accession":"SRR5813784","machine_type":"NextSeq 500","paired_end":true,"study_title":"IFNa impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing","study_abstract":"IFN-a impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing.","study_primary_id":"SRP111405"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP111405","sample_accession":"SRS2344233","experiment_accession":"SRX2992274","run_accession":"SRR5813790","machine_type":"NextSeq 500","paired_end":true,"study_title":"IFNa impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing","study_abstract":"IFN-a impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing.","study_primary_id":"SRP111405"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP111405","sample_accession":"SRS2344233","experiment_accession":"SRX2992276","run_accession":"SRR5813788","machine_type":"NextSeq 500","paired_end":true,"study_title":"IFNa impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing","study_abstract":"IFN-a impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing.","study_primary_id":"SRP111405"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP111405","sample_accession":"SRS2344233","experiment_accession":"SRX2992281","run_accession":"SRR5813783","machine_type":"NextSeq 500","paired_end":true,"study_title":"IFNa impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing","study_abstract":"IFN-a impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing.","study_primary_id":"SRP111405"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP111405","sample_accession":"SRS2344233","experiment_accession":"SRX2992283","run_accession":"SRR5813781","machine_type":"NextSeq 500","paired_end":true,"study_title":"IFNa impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing","study_abstract":"IFN-a impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing.","study_primary_id":"SRP111405"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP111405","sample_accession":"SRS2344233","experiment_accession":"SRX2992275","run_accession":"SRR5813789","machine_type":"NextSeq 500","paired_end":true,"study_title":"IFNa impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing","study_abstract":"IFN-a impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing.","study_primary_id":"SRP111405"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP111405","sample_accession":"SRS2344233","experiment_accession":"SRX2992277","run_accession":"SRR5813787","machine_type":"NextSeq 500","paired_end":true,"study_title":"IFNa impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing","study_abstract":"IFN-a impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing.","study_primary_id":"SRP111405"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP111405","sample_accession":"SRS2344233","experiment_accession":"SRX2992273","run_accession":"SRR5813791","machine_type":"NextSeq 500","paired_end":true,"study_title":"IFNa impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing","study_abstract":"IFN-a impairs autophagic degradation and promotes the autoreactivity of SLE monocytes through cell-autonomous mitochondrial DNA sensing.","study_primary_id":"SRP111405"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP113788","sample_accession":"SRS2393546","experiment_accession":"SRX3046330","run_accession":"SRR5879106","machine_type":"NextSeq 500","paired_end":false,"study_title":"Early transcriptome profiling of microRNA-mediated neuronal reprogramming [RNA-seq timecourse]","study_abstract":"Neuronal microRNAs, miR-9/9* and miR-124 (miR-9/9*-124), exert reprogramming activities to direct cell-fate conversion of adult human fibroblasts to post-mitotic neurons and enable the generation of discrete neuronal subtypes with additional transcription factors. Previously, the molecular events underlying the neurogenic switch mediated by microRNAs during neuronal reprogramming were unknown. Here, we systematically dissected the neurogenic state induced by miR-9/9*-124 alone and reveal the surprising capability of miR-9/9*-124 in coordinately stimulating the reconfiguration of chromatin accessibilities, DNA methylation and transcriptome, leading to the generation of functionally excitable neurons, yet unbiased towards a particular subtype-lineage. We show that the microRNA-induced neuronal state enables additional transcription factors, ISL1 and LHX3, to selectively commit conversion to a highly homogenous population of human spinal cord motor neurons. Taken together, our study reveals a modular synergism between microRNAs and transcription factors that allows lineage-specific neuronal reprogramming, providing a platform for generating distinct subtypes of human neurons. Overall design: Time series RNA-seq of miRNA-mediated neuronal reprogramming at post-induction day (PID) 0, 3, 6, 10, and 20.","study_primary_id":"SRP113788"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP113788","sample_accession":"SRS2393542","experiment_accession":"SRX3046326","run_accession":"SRR5879102","machine_type":"NextSeq 500","paired_end":false,"study_title":"Early transcriptome profiling of microRNA-mediated neuronal reprogramming [RNA-seq timecourse]","study_abstract":"Neuronal microRNAs, miR-9/9* and miR-124 (miR-9/9*-124), exert reprogramming activities to direct cell-fate conversion of adult human fibroblasts to post-mitotic neurons and enable the generation of discrete neuronal subtypes with additional transcription factors. Previously, the molecular events underlying the neurogenic switch mediated by microRNAs during neuronal reprogramming were unknown. Here, we systematically dissected the neurogenic state induced by miR-9/9*-124 alone and reveal the surprising capability of miR-9/9*-124 in coordinately stimulating the reconfiguration of chromatin accessibilities, DNA methylation and transcriptome, leading to the generation of functionally excitable neurons, yet unbiased towards a particular subtype-lineage. We show that the microRNA-induced neuronal state enables additional transcription factors, ISL1 and LHX3, to selectively commit conversion to a highly homogenous population of human spinal cord motor neurons. Taken together, our study reveals a modular synergism between microRNAs and transcription factors that allows lineage-specific neuronal reprogramming, providing a platform for generating distinct subtypes of human neurons. Overall design: Time series RNA-seq of miRNA-mediated neuronal reprogramming at post-induction day (PID) 0, 3, 6, 10, and 20.","study_primary_id":"SRP113788"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP113788","sample_accession":"SRS2393548","experiment_accession":"SRX3046332","run_accession":"SRR5879107","machine_type":"NextSeq 500","paired_end":false,"study_title":"Early transcriptome profiling of microRNA-mediated neuronal reprogramming [RNA-seq timecourse]","study_abstract":"Neuronal microRNAs, miR-9/9* and miR-124 (miR-9/9*-124), exert reprogramming activities to direct cell-fate conversion of adult human fibroblasts to post-mitotic neurons and enable the generation of discrete neuronal subtypes with additional transcription factors. Previously, the molecular events underlying the neurogenic switch mediated by microRNAs during neuronal reprogramming were unknown. Here, we systematically dissected the neurogenic state induced by miR-9/9*-124 alone and reveal the surprising capability of miR-9/9*-124 in coordinately stimulating the reconfiguration of chromatin accessibilities, DNA methylation and transcriptome, leading to the generation of functionally excitable neurons, yet unbiased towards a particular subtype-lineage. We show that the microRNA-induced neuronal state enables additional transcription factors, ISL1 and LHX3, to selectively commit conversion to a highly homogenous population of human spinal cord motor neurons. Taken together, our study reveals a modular synergism between microRNAs and transcription factors that allows lineage-specific neuronal reprogramming, providing a platform for generating distinct subtypes of human neurons. Overall design: Time series RNA-seq of miRNA-mediated neuronal reprogramming at post-induction day (PID) 0, 3, 6, 10, and 20.","study_primary_id":"SRP113788"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP113788","sample_accession":"SRS2393540","experiment_accession":"SRX3046324","run_accession":"SRR5879100","machine_type":"NextSeq 500","paired_end":false,"study_title":"Early transcriptome profiling of microRNA-mediated neuronal reprogramming [RNA-seq timecourse]","study_abstract":"Neuronal microRNAs, miR-9/9* and miR-124 (miR-9/9*-124), exert reprogramming activities to direct cell-fate conversion of adult human fibroblasts to post-mitotic neurons and enable the generation of discrete neuronal subtypes with additional transcription factors. Previously, the molecular events underlying the neurogenic switch mediated by microRNAs during neuronal reprogramming were unknown. Here, we systematically dissected the neurogenic state induced by miR-9/9*-124 alone and reveal the surprising capability of miR-9/9*-124 in coordinately stimulating the reconfiguration of chromatin accessibilities, DNA methylation and transcriptome, leading to the generation of functionally excitable neurons, yet unbiased towards a particular subtype-lineage. We show that the microRNA-induced neuronal state enables additional transcription factors, ISL1 and LHX3, to selectively commit conversion to a highly homogenous population of human spinal cord motor neurons. Taken together, our study reveals a modular synergism between microRNAs and transcription factors that allows lineage-specific neuronal reprogramming, providing a platform for generating distinct subtypes of human neurons. Overall design: Time series RNA-seq of miRNA-mediated neuronal reprogramming at post-induction day (PID) 0, 3, 6, 10, and 20.","study_primary_id":"SRP113788"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP113788","sample_accession":"SRS2393539","experiment_accession":"SRX3046323","run_accession":"SRR5879099","machine_type":"NextSeq 500","paired_end":false,"study_title":"Early transcriptome profiling of microRNA-mediated neuronal reprogramming [RNA-seq timecourse]","study_abstract":"Neuronal microRNAs, miR-9/9* and miR-124 (miR-9/9*-124), exert reprogramming activities to direct cell-fate conversion of adult human fibroblasts to post-mitotic neurons and enable the generation of discrete neuronal subtypes with additional transcription factors. Previously, the molecular events underlying the neurogenic switch mediated by microRNAs during neuronal reprogramming were unknown. Here, we systematically dissected the neurogenic state induced by miR-9/9*-124 alone and reveal the surprising capability of miR-9/9*-124 in coordinately stimulating the reconfiguration of chromatin accessibilities, DNA methylation and transcriptome, leading to the generation of functionally excitable neurons, yet unbiased towards a particular subtype-lineage. We show that the microRNA-induced neuronal state enables additional transcription factors, ISL1 and LHX3, to selectively commit conversion to a highly homogenous population of human spinal cord motor neurons. Taken together, our study reveals a modular synergism between microRNAs and transcription factors that allows lineage-specific neuronal reprogramming, providing a platform for generating distinct subtypes of human neurons. Overall design: Time series RNA-seq of miRNA-mediated neuronal reprogramming at post-induction day (PID) 0, 3, 6, 10, and 20.","study_primary_id":"SRP113788"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP113788","sample_accession":"SRS2393543","experiment_accession":"SRX3046327","run_accession":"SRR5879103","machine_type":"NextSeq 500","paired_end":false,"study_title":"Early transcriptome profiling of microRNA-mediated neuronal reprogramming [RNA-seq timecourse]","study_abstract":"Neuronal microRNAs, miR-9/9* and miR-124 (miR-9/9*-124), exert reprogramming activities to direct cell-fate conversion of adult human fibroblasts to post-mitotic neurons and enable the generation of discrete neuronal subtypes with additional transcription factors. Previously, the molecular events underlying the neurogenic switch mediated by microRNAs during neuronal reprogramming were unknown. Here, we systematically dissected the neurogenic state induced by miR-9/9*-124 alone and reveal the surprising capability of miR-9/9*-124 in coordinately stimulating the reconfiguration of chromatin accessibilities, DNA methylation and transcriptome, leading to the generation of functionally excitable neurons, yet unbiased towards a particular subtype-lineage. We show that the microRNA-induced neuronal state enables additional transcription factors, ISL1 and LHX3, to selectively commit conversion to a highly homogenous population of human spinal cord motor neurons. Taken together, our study reveals a modular synergism between microRNAs and transcription factors that allows lineage-specific neuronal reprogramming, providing a platform for generating distinct subtypes of human neurons. Overall design: Time series RNA-seq of miRNA-mediated neuronal reprogramming at post-induction day (PID) 0, 3, 6, 10, and 20.","study_primary_id":"SRP113788"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP113788","sample_accession":"SRS2393544","experiment_accession":"SRX3046328","run_accession":"SRR5879104","machine_type":"NextSeq 500","paired_end":false,"study_title":"Early transcriptome profiling of microRNA-mediated neuronal reprogramming [RNA-seq timecourse]","study_abstract":"Neuronal microRNAs, miR-9/9* and miR-124 (miR-9/9*-124), exert reprogramming activities to direct cell-fate conversion of adult human fibroblasts to post-mitotic neurons and enable the generation of discrete neuronal subtypes with additional transcription factors. Previously, the molecular events underlying the neurogenic switch mediated by microRNAs during neuronal reprogramming were unknown. Here, we systematically dissected the neurogenic state induced by miR-9/9*-124 alone and reveal the surprising capability of miR-9/9*-124 in coordinately stimulating the reconfiguration of chromatin accessibilities, DNA methylation and transcriptome, leading to the generation of functionally excitable neurons, yet unbiased towards a particular subtype-lineage. We show that the microRNA-induced neuronal state enables additional transcription factors, ISL1 and LHX3, to selectively commit conversion to a highly homogenous population of human spinal cord motor neurons. Taken together, our study reveals a modular synergism between microRNAs and transcription factors that allows lineage-specific neuronal reprogramming, providing a platform for generating distinct subtypes of human neurons. Overall design: Time series RNA-seq of miRNA-mediated neuronal reprogramming at post-induction day (PID) 0, 3, 6, 10, and 20.","study_primary_id":"SRP113788"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP113788","sample_accession":"SRS2393538","experiment_accession":"SRX3046322","run_accession":"SRR5879098","machine_type":"NextSeq 500","paired_end":false,"study_title":"Early transcriptome profiling of microRNA-mediated neuronal reprogramming [RNA-seq timecourse]","study_abstract":"Neuronal microRNAs, miR-9/9* and miR-124 (miR-9/9*-124), exert reprogramming activities to direct cell-fate conversion of adult human fibroblasts to post-mitotic neurons and enable the generation of discrete neuronal subtypes with additional transcription factors. Previously, the molecular events underlying the neurogenic switch mediated by microRNAs during neuronal reprogramming were unknown. Here, we systematically dissected the neurogenic state induced by miR-9/9*-124 alone and reveal the surprising capability of miR-9/9*-124 in coordinately stimulating the reconfiguration of chromatin accessibilities, DNA methylation and transcriptome, leading to the generation of functionally excitable neurons, yet unbiased towards a particular subtype-lineage. We show that the microRNA-induced neuronal state enables additional transcription factors, ISL1 and LHX3, to selectively commit conversion to a highly homogenous population of human spinal cord motor neurons. Taken together, our study reveals a modular synergism between microRNAs and transcription factors that allows lineage-specific neuronal reprogramming, providing a platform for generating distinct subtypes of human neurons. Overall design: Time series RNA-seq of miRNA-mediated neuronal reprogramming at post-induction day (PID) 0, 3, 6, 10, and 20.","study_primary_id":"SRP113788"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP113788","sample_accession":"SRS2393545","experiment_accession":"SRX3046329","run_accession":"SRR5879105","machine_type":"NextSeq 500","paired_end":false,"study_title":"Early transcriptome profiling of microRNA-mediated neuronal reprogramming [RNA-seq timecourse]","study_abstract":"Neuronal microRNAs, miR-9/9* and miR-124 (miR-9/9*-124), exert reprogramming activities to direct cell-fate conversion of adult human fibroblasts to post-mitotic neurons and enable the generation of discrete neuronal subtypes with additional transcription factors. Previously, the molecular events underlying the neurogenic switch mediated by microRNAs during neuronal reprogramming were unknown. Here, we systematically dissected the neurogenic state induced by miR-9/9*-124 alone and reveal the surprising capability of miR-9/9*-124 in coordinately stimulating the reconfiguration of chromatin accessibilities, DNA methylation and transcriptome, leading to the generation of functionally excitable neurons, yet unbiased towards a particular subtype-lineage. We show that the microRNA-induced neuronal state enables additional transcription factors, ISL1 and LHX3, to selectively commit conversion to a highly homogenous population of human spinal cord motor neurons. Taken together, our study reveals a modular synergism between microRNAs and transcription factors that allows lineage-specific neuronal reprogramming, providing a platform for generating distinct subtypes of human neurons. Overall design: Time series RNA-seq of miRNA-mediated neuronal reprogramming at post-induction day (PID) 0, 3, 6, 10, and 20.","study_primary_id":"SRP113788"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP113788","sample_accession":"SRS2393541","experiment_accession":"SRX3046325","run_accession":"SRR5879101","machine_type":"NextSeq 500","paired_end":false,"study_title":"Early transcriptome profiling of microRNA-mediated neuronal reprogramming [RNA-seq timecourse]","study_abstract":"Neuronal microRNAs, miR-9/9* and miR-124 (miR-9/9*-124), exert reprogramming activities to direct cell-fate conversion of adult human fibroblasts to post-mitotic neurons and enable the generation of discrete neuronal subtypes with additional transcription factors. Previously, the molecular events underlying the neurogenic switch mediated by microRNAs during neuronal reprogramming were unknown. Here, we systematically dissected the neurogenic state induced by miR-9/9*-124 alone and reveal the surprising capability of miR-9/9*-124 in coordinately stimulating the reconfiguration of chromatin accessibilities, DNA methylation and transcriptome, leading to the generation of functionally excitable neurons, yet unbiased towards a particular subtype-lineage. We show that the microRNA-induced neuronal state enables additional transcription factors, ISL1 and LHX3, to selectively commit conversion to a highly homogenous population of human spinal cord motor neurons. Taken together, our study reveals a modular synergism between microRNAs and transcription factors that allows lineage-specific neuronal reprogramming, providing a platform for generating distinct subtypes of human neurons. Overall design: Time series RNA-seq of miRNA-mediated neuronal reprogramming at post-induction day (PID) 0, 3, 6, 10, and 20.","study_primary_id":"SRP113788"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP117227","sample_accession":"SRS2505389","experiment_accession":"SRX3175508","run_accession":"SRR6024767","machine_type":"Illumina HiSeq 4000","paired_end":true,"study_title":"PINT circular RNA Encodes a Novel Tumor Suppressive Protein in human Cells","study_abstract":"Human glioblastoma U251 and U373 cells were infected by lentivirus of PCDH-flag and PCDH-87aa .The total RNAs were extracted By Trizol . Then total RNAs were enriched for deep sequencing to detect the expression profile of RNA .","study_primary_id":"SRP117227"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP117227","sample_accession":"SRS2505388","experiment_accession":"SRX3175507","run_accession":"SRR6024768","machine_type":"Illumina HiSeq 4000","paired_end":true,"study_title":"PINT circular RNA Encodes a Novel Tumor Suppressive Protein in human Cells","study_abstract":"Human glioblastoma U251 and U373 cells were infected by lentivirus of PCDH-flag and PCDH-87aa .The total RNAs were extracted By Trizol . Then total RNAs were enriched for deep sequencing to detect the expression profile of RNA .","study_primary_id":"SRP117227"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP117227","sample_accession":"SRS2505387","experiment_accession":"SRX3175506","run_accession":"SRR6024769","machine_type":"Illumina HiSeq 4000","paired_end":true,"study_title":"PINT circular RNA Encodes a Novel Tumor Suppressive Protein in human Cells","study_abstract":"Human glioblastoma U251 and U373 cells were infected by lentivirus of PCDH-flag and PCDH-87aa .The total RNAs were extracted By Trizol . Then total RNAs were enriched for deep sequencing to detect the expression profile of RNA .","study_primary_id":"SRP117227"} {"taxon_id":9606,"library_source":"TRANSCRIPTOMIC","study_accession":"SRP117227","sample_accession":"SRS2505386","experiment_accession":"SRX3175505","run_accession":"SRR6024770","machine_type":"Illumina HiSeq 4000","paired_end":true,"study_title":"PINT circular RNA Encodes a Novel Tumor Suppressive Protein in human Cells","study_abstract":"Human glioblastoma U251 and U373 cells were infected by lentivirus of PCDH-flag and PCDH-87aa .The total RNAs were extracted By Trizol . Then total RNAs were enriched for deep sequencing to detect the expression profile of RNA .","study_primary_id":"SRP117227"}