{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Qiu X"],"funding":["Zhejiang Provincial Postdoctoral Science Foundation","National Key R&D Program of China","Shuguang Project","Natural Science Fund for Excellent Young Scholars of China","China Postdoctoral Science Foundation","National Natural Science Foundation of China","Shanghai Research Center for Endocrine and Metabolic Diseases","Major Natural Science Project of the Scientific Research and Innovation Plan of Shanghai Municipal Commission of Education","Innovative research team of high-level local universities in Shanghai","Zhejiang Provincial Natural Science Foundation","Construction Fund of Medical Key Disciplines of Hangzhou"],"pagination":["e177980"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12646663"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["135(23)"],"pubmed_abstract":["Impaired glucose-stimulated insulin secretion (GSIS) is a hallmark of β cell dysfunction in diabetes. Epigenetic mechanisms govern cellular glucose sensing and GSIS by β cells, but they remain incompletely defined. Here, we found that BAF60a functions as a chromatin regulator that sustains biphasic GSIS and preserves β cell function under metabolic stress conditions. BAF60a was downregulated in β cells from obese and diabetic mice, monkeys, and humans. β cell-specific inactivation of BAF60a in adult mice impaired GSIS, leading to hyperglycemia and glucose intolerance. Conversely, restoring BAF60a expression improved β cell function and systemic glucose homeostasis. Mechanistically, BAF60a physically interacted with Nkx6.1 to selectively modulate chromatin accessibility and transcriptional "],"journal":["The Journal of clinical investigation"],"pubmed_title":["BAF60a-dependent chromatin remodeling preserves β cell function and contributes to the therapeutic benefits of GLP-1R agonists."],"pmcid":["PMC12646663"],"funding_grant_id":["2023ZKZD17","LHDMD24H030001,LZ21H070001,LHDMD22H02001","SHSMU-ZDCX20212700","81722012","No.2025HZZD06","ZJ2022117","21SG11","2022ZZ01002","2018YFA0800403,2021YFC2701903","2022M723284","82425012,92457301,32471170,91857110,81722012,82325010,82300893,82500965"],"pubmed_authors":["Shi M","Zhang R","Ding W","Qiu X","Wang Q","Piao HL","Zheng M","Guo G","Chen W","Wang W","Meng ZX","Wang RR","Jin L","Pan X","Yan J","Li C","Yan S","Chen H","Liang B","Zhang W","Hu C","Luo P","Yang Y","Ji X","Zhang Z","Fu H","Zhu L","Yan D","Wu QQ","Zhu S"],"additional_accession":[]},"is_claimable":false,"name":"BAF60a-dependent chromatin remodeling preserves β cell function and contributes to the therapeutic benefits of GLP-1R agonists.","description":"Impaired glucose-stimulated insulin secretion (GSIS) is a hallmark of β cell dysfunction in diabetes. Epigenetic mechanisms govern cellular glucose sensing and GSIS by β cells, but they remain incompletely defined. Here, we found that BAF60a functions as a chromatin regulator that sustains biphasic GSIS and preserves β cell function under metabolic stress conditions. BAF60a was downregulated in β cells from obese and diabetic mice, monkeys, and humans. β cell-specific inactivation of BAF60a in adult mice impaired GSIS, leading to hyperglycemia and glucose intolerance. Conversely, restoring BAF60a expression improved β cell function and systemic glucose homeostasis. Mechanistically, BAF60a physically interacted with Nkx6.1 to selectively modulate chromatin accessibility and transcriptional ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Dec","modification":"2026-06-05T19:13:04.449Z","creation":"2026-05-20T03:14:51.705Z"},"accession":"S-EPMC12646663","cross_references":{"pubmed":["41052246"],"doi":["10.1172/JCI177980"]}}