{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Prefontaine C"],"funding":["Canada Foundation for Innovation John R. Evans Leaders Fund","Canadian Institutes of Health Research and Breakthrough T1D","Canadian Islet Research and Training Network and NSERC-CREATE program","Institute of Nutrition, Metabolism and Diabetes","Breakthrough T1D Advanced Postdoctoral Fellowship","Manitoba Medical Service Foundation","Canadian Islet Research and Training Network and Breakthrough T1D","Diabetes Canada"],"pagination":["421-435"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12779684"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["69(2)"],"pubmed_abstract":["<h4>Aims/hypothesis</h4>Residual pancreatic beta cells in type 1 diabetes show reduced insulin production but the mechanisms remain unclear. Beta cells undergo stress responses during type 1 diabetes, including endoplasmic reticulum (ER) stress and DNA damage-associated senescence, which may affect insulin production. ER stress reduces insulin production but whether senescence disrupts insulin production in human beta cells has not been investigated.<h4>Methods</h4>DNA damage-mediated senescence was induced using bleomycin in human donor islets. Relative levels of prohormone convertase 1/3 (PC1/3), prohormone convertase 2 (PC2), carboxypeptidase E (CPE) and the endogenous PC1/3 inhibitor, proprotein convertase subtilisin/kexin type 1 inhibitor (proSAAS), were quantified by western blot. Le"],"journal":["Diabetologia"],"pubmed_title":["Insulin production is sustained during DNA damage-mediated senescence in adult human beta cells."],"pmcid":["PMC12779684"],"funding_grant_id":["43168","3-APF-2022–1141-A-N","PJT-479641","2023 Allen Rouse Basic Science Career Development","MSc training award","197485","OG-3-22-5694-PT","3-APF-2022-1141-A-N","postdoctoral fellowship award","TDP-186359","3-COE-2022-1103-M-B","PJT-485915"],"pubmed_authors":["Thompson PJ","Chen YC","Prefontaine C","Pipella J","Rampazzo Morelli N","Verchere CB"],"additional_accession":[]},"is_claimable":false,"name":"Insulin production is sustained during DNA damage-mediated senescence in adult human beta cells.","description":"<h4>Aims/hypothesis</h4>Residual pancreatic beta cells in type 1 diabetes show reduced insulin production but the mechanisms remain unclear. Beta cells undergo stress responses during type 1 diabetes, including endoplasmic reticulum (ER) stress and DNA damage-associated senescence, which may affect insulin production. ER stress reduces insulin production but whether senescence disrupts insulin production in human beta cells has not been investigated.<h4>Methods</h4>DNA damage-mediated senescence was induced using bleomycin in human donor islets. Relative levels of prohormone convertase 1/3 (PC1/3), prohormone convertase 2 (PC2), carboxypeptidase E (CPE) and the endogenous PC1/3 inhibitor, proprotein convertase subtilisin/kexin type 1 inhibitor (proSAAS), were quantified by western blot. Le","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Feb","modification":"2026-07-15T07:48:54.114Z","creation":"2026-07-01T03:07:42.164Z"},"accession":"S-EPMC12779684","cross_references":{"pubmed":["41231256"],"doi":["10.1007/s00125-025-06603-3"]}}