{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Nagy ZS"],"funding":["NCRR NIH HHS","NIAID NIH HHS","NIGMS NIH HHS"],"pagination":["e57326"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3581501"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(2)"],"pubmed_abstract":["IL-2 is the primary growth factor for promoting survival and proliferation of activated T cells that occurs following engagement of the Janus Kinase (JAK)1-3/and Signal Transducer and Activator of Transcription (STAT) 5 signaling pathway. STAT5 has two isoforms: STAT5A and STAT5B (commonly referred to as STAT5) which, in T cells, play redundant roles transcribing cell cycle and survival genes. As such, inhibition of STAT5 by a variety of mechanisms can rapidly induce apoptosis in certain lymphoid tumor cells, suggesting that it and its target genes represent therapeutic targets to control certain lymphoid diseases. To search for these molecules we aligned IL-2 regulated genes detected by Affymetrix gene expression microarrays with the STAT5 cistrome identified by chip-on-ChIP analysis in a"],"journal":["PloS one"],"pubmed_title":["Genome wide mapping reveals PDE4B as an IL-2 induced STAT5 target gene in activated human PBMCs and lymphoid cancer cells."],"pmcid":["PMC3581501"],"funding_grant_id":["AI053566","G12 RR008124","S06 GM008012","5G12RR008124","S06 GM008012-37","R01 AI053566"],"pubmed_authors":["Nagy L","Rodriguez G","Ross JA","Kirken RA","Nagy ZS","Szeles L","Balint BL"],"additional_accession":[]},"is_claimable":false,"name":"Genome wide mapping reveals PDE4B as an IL-2 induced STAT5 target gene in activated human PBMCs and lymphoid cancer cells.","description":"IL-2 is the primary growth factor for promoting survival and proliferation of activated T cells that occurs following engagement of the Janus Kinase (JAK)1-3/and Signal Transducer and Activator of Transcription (STAT) 5 signaling pathway. STAT5 has two isoforms: STAT5A and STAT5B (commonly referred to as STAT5) which, in T cells, play redundant roles transcribing cell cycle and survival genes. As such, inhibition of STAT5 by a variety of mechanisms can rapidly induce apoptosis in certain lymphoid tumor cells, suggesting that it and its target genes represent therapeutic targets to control certain lymphoid diseases. To search for these molecules we aligned IL-2 regulated genes detected by Affymetrix gene expression microarrays with the STAT5 cistrome identified by chip-on-ChIP analysis in a","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013","modification":"2026-04-07T16:45:23.309Z","creation":"2019-03-26T23:19:56Z"},"accession":"S-EPMC3581501","cross_references":{"pubmed":["23451206"],"doi":["10.1371/journal.pone.0057326"]}}