{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Patel CH"],"funding":["NIAID NIH HHS","HHS | NIH | National Institute of Biomedical Imaging and Bioengineering","HHS | NIH | National Institute of Allergy and Infectious Diseases"],"pagination":["2287-2291"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10065985"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["209(12)"],"pubmed_abstract":["The mechanistic target of rapamycin is an essential regulator of T cell metabolism and differentiation. In this study, we demonstrate that serum- and glucocorticoid-regulated kinase 1 (SGK1), a downstream node of mechanistic target of rapamycin complex 2 signaling, represses memory CD8+ T cell differentiation. During acute infections, murine SGK1-deficient CD8+ T cells adopt an early memory precursor phenotype leading to more long-lived memory T cells. Thus, SGK1-deficient CD8+ T cells demonstrate an enhanced recall capacity in response to reinfection and can readily reject tumors. Mechanistically, activation of SGK1-deficient CD8+ T cells results in decreased Foxo1 phosphorylation and increased nuclear translocation of Foxo1 to promote early memory development. Overall, SGK1 might prove t"],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pubmed_title":["Cutting Edge: mTORC2 Regulates CD8+ Effector and Memory T Cell Differentiation through Serum and Glucocorticoid Kinase 1."],"pmcid":["PMC10065985"],"funding_grant_id":["P41EB028239","R01AI07761","R01 AI077610"],"pubmed_authors":["Wen J","Blosser RL","Patel CH","Sun IH","Tam AJ","Powell JD","Oh MH","Xu W","Sun IM","Heikamp EB"],"additional_accession":[]},"is_claimable":false,"name":"Cutting Edge: mTORC2 Regulates CD8+ Effector and Memory T Cell Differentiation through Serum and Glucocorticoid Kinase 1.","description":"The mechanistic target of rapamycin is an essential regulator of T cell metabolism and differentiation. In this study, we demonstrate that serum- and glucocorticoid-regulated kinase 1 (SGK1), a downstream node of mechanistic target of rapamycin complex 2 signaling, represses memory CD8+ T cell differentiation. During acute infections, murine SGK1-deficient CD8+ T cells adopt an early memory precursor phenotype leading to more long-lived memory T cells. Thus, SGK1-deficient CD8+ T cells demonstrate an enhanced recall capacity in response to reinfection and can readily reject tumors. Mechanistically, activation of SGK1-deficient CD8+ T cells results in decreased Foxo1 phosphorylation and increased nuclear translocation of Foxo1 to promote early memory development. Overall, SGK1 might prove t","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Dec","modification":"2025-04-04T11:20:56.657Z","creation":"2025-04-04T11:20:56.657Z"},"accession":"S-EPMC10065985","cross_references":{"pubmed":["36469844"],"doi":["10.4049/jimmunol.2100669"]}}