{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang Y"],"funding":["NIAID NIH HHS","National Institutes of Health","NIAMS NIH HHS","NIGMS NIH HHS"],"pagination":["600-612"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5772774"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["20(3)"],"pubmed_abstract":["The development of CD1d-restricted invariant natural killer T (iNKT) cells, a population that is critical for both innate and adaptive immunity, is regulated by multiple transcription factors, but the molecular mechanisms underlying how the transcriptional activation of these factors are regulated during iNKT development remain largely unknown. We found that the histone acetyltransferase general control non-derepressible 5 (GCN5) is essential for iNKT cell development during the maturation stage. GCN5 deficiency blocked iNKT cell development in a cell-intrinsic manner. At the molecular level, GCN5 is a specific lysine acetyltransferase of early growth responsive gene 2 (EGR2), a transcription factor required for iNKT cell development. GCN5-mediated acetylation positively regulated EGR2 transcriptional activity, and both genetic and pharmacological GCN5 suppression specifically inhibited the transcription of EGR2 target genes in iNKT cells, including Runx1, promyelocytic leukemia zinc finger protein (PLZF), interleukin (IL)-2Rb, and T-bet. Therefore, our study revealed GCN5-mediated EGR2 acetylation as a molecular mechanism that regulates iNKT development."],"journal":["Cell reports"],"pubmed_title":["The Lysine Acetyltransferase GCN5 Is Required for iNKT Cell Development through EGR2 Acetylation."],"pmcid":["PMC5772774"],"funding_grant_id":["R01 GM067718","AR006634","AI043407","R01 AI043407","R01 AI079056","R01 AI108634","AI108634","AI079056","R56 AI079056","R01 AR066634"],"pubmed_authors":["Gao B","Li HB","Kong Q","Fang D","Yun C","Wang CR","Wang J","Zhang Y","Zhao F","Wang Y","Xu X","Xu Y","Dent SYR"],"additional_accession":[]},"is_claimable":false,"name":"The Lysine Acetyltransferase GCN5 Is Required for iNKT Cell Development through EGR2 Acetylation.","description":"The development of CD1d-restricted invariant natural killer T (iNKT) cells, a population that is critical for both innate and adaptive immunity, is regulated by multiple transcription factors, but the molecular mechanisms underlying how the transcriptional activation of these factors are regulated during iNKT development remain largely unknown. We found that the histone acetyltransferase general control non-derepressible 5 (GCN5) is essential for iNKT cell development during the maturation stage. GCN5 deficiency blocked iNKT cell development in a cell-intrinsic manner. At the molecular level, GCN5 is a specific lysine acetyltransferase of early growth responsive gene 2 (EGR2), a transcription factor required for iNKT cell development. GCN5-mediated acetylation positively regulated EGR2 transcriptional activity, and both genetic and pharmacological GCN5 suppression specifically inhibited the transcription of EGR2 target genes in iNKT cells, including Runx1, promyelocytic leukemia zinc finger protein (PLZF), interleukin (IL)-2Rb, and T-bet. Therefore, our study revealed GCN5-mediated EGR2 acetylation as a molecular mechanism that regulates iNKT development.","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Jul","modification":"2026-05-05T22:10:05.759Z","creation":"2019-03-26T23:46:31Z"},"accession":"S-EPMC5772774","cross_references":{"pubmed":["28723564"],"doi":["10.1016/j.celrep.2017.06.065"]}}