{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["He Z"],"funding":["NIAID NIH HHS","NCI NIH HHS"],"pagination":["760-769"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6344289"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["202(3)"],"pubmed_abstract":["SRC3, a highly conserved member of the steroid receptor coactivator (SRC) family, is recruited by transcription factors to regulate cellular function. Previously, we demonstrated that SRC1, another highly conserved member of the SRC family, interacts with RORγt to regulate Th17 differentiation. However, the relationship between SRC1 and SRC3 in the regulation of Th17 cell function remains unknown. In this study, we demonstrate that mouse SRC3 interacts with RORγt in Th17 cells but not in thymocytes. In addition, Src3-/- mice exhibited defective Th17 differentiation and induction of experimental autoimmune encephalomyelitis but normal thymocyte development. Furthermore, a K313 to arginine mutation of RORγt (RORγt-K313R), which disrupts the interaction of RORγt with SRC3 but not with SRC1, i"],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pubmed_title":["SRC3 Is a Cofactor for RORγt in Th17 Differentiation but Not Thymocyte Development."],"pmcid":["PMC6344289"],"funding_grant_id":["R01 AI083432","R01 AI109644","P30 CA033572"],"pubmed_authors":["Du Q","Gwack Y","He Z","Zhang J","Xu J","Sun Z"],"additional_accession":[]},"is_claimable":false,"name":"SRC3 Is a Cofactor for RORγt in Th17 Differentiation but Not Thymocyte Development.","description":"SRC3, a highly conserved member of the steroid receptor coactivator (SRC) family, is recruited by transcription factors to regulate cellular function. Previously, we demonstrated that SRC1, another highly conserved member of the SRC family, interacts with RORγt to regulate Th17 differentiation. However, the relationship between SRC1 and SRC3 in the regulation of Th17 cell function remains unknown. In this study, we demonstrate that mouse SRC3 interacts with RORγt in Th17 cells but not in thymocytes. In addition, Src3-/- mice exhibited defective Th17 differentiation and induction of experimental autoimmune encephalomyelitis but normal thymocyte development. Furthermore, a K313 to arginine mutation of RORγt (RORγt-K313R), which disrupts the interaction of RORγt with SRC3 but not with SRC1, i","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Feb","modification":"2025-04-19T16:36:35.514Z","creation":"2020-10-02T07:33:38Z"},"accession":"S-EPMC6344289","cross_references":{"pubmed":["30567733"],"doi":["10.4049/jimmunol.1801187"]}}