{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Miyachi Y"],"funding":["National Institute of Diabetes and Digestive and Kidney Diseases","MSD Life Science foundation","Uehara Memorial Foundation","Mochida Memorial Foundation for Medical and Pharmaceutical Research","Japan Society for the Promotion of Science"],"pagination":["e0260526"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8629236"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(11)"],"pubmed_abstract":["Beta cell failure is a critical feature of diabetes. It includes defects of insulin production, secretion, and altered numbers of hormone-producing cells. In previous work, we have shown that beta cell failure is mechanistically linked to loss of Foxo1 function. This loss of function likely results from increased Foxo1 protein degradation, due to hyperacetylation of Foxo1 from increased nutrient turnover. To understand the mechanisms of Foxo1-related beta cell failure, we performed genome-wide analyses of its target genes, and identified putative mediators of sub-phenotypes of cellular dysfunction. Chromatin immunoprecipitation analyses demonstrated a striking pattern of Foxo1 binding to the promoters of a cluster of aldo-ketoreductases on chromosome 13: Akr1c12, Akr1c13, Akr1c19. Of these"],"journal":["PloS one"],"pubmed_title":["Aldo-ketoreductase 1c19 ablation does not affect insulin secretion in murine islets."],"pmcid":["PMC8629236"],"funding_grant_id":["DK63618","21K20934","DK64819"],"pubmed_authors":["Miyachi Y","Accili D","Son J","Kuo T"],"additional_accession":[]},"is_claimable":false,"name":"Aldo-ketoreductase 1c19 ablation does not affect insulin secretion in murine islets.","description":"Beta cell failure is a critical feature of diabetes. It includes defects of insulin production, secretion, and altered numbers of hormone-producing cells. In previous work, we have shown that beta cell failure is mechanistically linked to loss of Foxo1 function. This loss of function likely results from increased Foxo1 protein degradation, due to hyperacetylation of Foxo1 from increased nutrient turnover. To understand the mechanisms of Foxo1-related beta cell failure, we performed genome-wide analyses of its target genes, and identified putative mediators of sub-phenotypes of cellular dysfunction. Chromatin immunoprecipitation analyses demonstrated a striking pattern of Foxo1 binding to the promoters of a cluster of aldo-ketoreductases on chromosome 13: Akr1c12, Akr1c13, Akr1c19. Of these","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021","modification":"2025-04-04T14:54:41.948Z","creation":"2022-02-11T13:47:07.145Z"},"accession":"S-EPMC8629236","cross_references":{"pubmed":["34843575"],"doi":["10.1371/journal.pone.0260526"]}}