{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cunningham CA"],"funding":["NIAID NIH HHS"],"pagination":["4003-13"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4868786"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["196(10)"],"pubmed_abstract":["The scaffold molecule POSH is crucial for the regulation of proliferation and effector function in CD8(+) T cells. However, its role in CD4(+) T cells is not known. In this study, we found that disruption of the POSH scaffold complex established a transcriptional profile that strongly skewed differentiation toward Th2, led to decreased survival, and had no effect on cell cycle entry. This is in stark contrast to CD8(+) T cells in which POSH regulates cell cycle and does not affect survival. Disruption of POSH in CD4(+) T cells resulted in the loss of Tak1-dependent activation of JNK1/2 and Tak1-mediated survival. However, in CD8(+) T cells, POSH regulates only JNK1. Remarkably, each type of T cell had a unique composition of the POSH scaffold complex and distinct posttranslational modifications of POSH. These data indicate that the mechanism that regulates POSH function in CD4(+) T cells is different from CD8(+) T cells. All together, these data strongly suggest that POSH is essential for the integration of cell-type-specific signals that regulate the differentiation, survival, and function of T cells."],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pubmed_title":["POSH Regulates CD4+ T Cell Differentiation and Survival."],"pmcid":["PMC4868786"],"funding_grant_id":["R56 AI110420","R01 AI110420"],"pubmed_authors":["Teixeiro E","Guan Y","Cardwell LN","Cunningham CA","Daniels MA"],"additional_accession":[]},"is_claimable":false,"name":"POSH Regulates CD4+ T Cell Differentiation and Survival.","description":"The scaffold molecule POSH is crucial for the regulation of proliferation and effector function in CD8(+) T cells. However, its role in CD4(+) T cells is not known. In this study, we found that disruption of the POSH scaffold complex established a transcriptional profile that strongly skewed differentiation toward Th2, led to decreased survival, and had no effect on cell cycle entry. This is in stark contrast to CD8(+) T cells in which POSH regulates cell cycle and does not affect survival. Disruption of POSH in CD4(+) T cells resulted in the loss of Tak1-dependent activation of JNK1/2 and Tak1-mediated survival. However, in CD8(+) T cells, POSH regulates only JNK1. Remarkably, each type of T cell had a unique composition of the POSH scaffold complex and distinct posttranslational modifications of POSH. These data indicate that the mechanism that regulates POSH function in CD4(+) T cells is different from CD8(+) T cells. All together, these data strongly suggest that POSH is essential for the integration of cell-type-specific signals that regulate the differentiation, survival, and function of T cells.","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 May","modification":"2025-04-29T10:14:17.13Z","creation":"2019-03-27T02:13:46Z"},"accession":"S-EPMC4868786","cross_references":{"pubmed":["27084103"],"doi":["10.4049/jimmunol.1501728"]}}