{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Bramswig NC"],"funding":["NIDDK NIH HHS","NCRR NIH HHS"],"pagination":["1275-84"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3582140"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["123(3)"],"pubmed_abstract":["Insulin-secreting β cells and glucagon-secreting α cells maintain physiological blood glucose levels, and their malfunction drives diabetes development. Using ChIP sequencing and RNA sequencing analysis, we determined the epigenetic and transcriptional landscape of human pancreatic α, β, and exocrine cells. We found that, compared with exocrine and β cells, differentiated α cells exhibited many more genes bivalently marked by the activating H3K4me3 and repressing H3K27me3 histone modifications. This was particularly true for β cell signature genes involved in transcriptional regulation. Remarkably, thousands of these genes were in a monovalent state in β cells, carrying only the activating or repressing mark. Our epigenomic findings suggested that α to β cell reprogramming could be promote"],"journal":["The Journal of clinical investigation"],"pubmed_title":["Epigenomic plasticity enables human pancreatic α to β cell reprogramming."],"pmcid":["PMC3582140"],"funding_grant_id":["U01DK089529","R01 DK088383","R01DK088383","U01 DK089529","U01 DK070430","U01DK089569","U01 DK089569","U42 RR006042"],"pubmed_authors":["Schug J","Naji A","Everett LJ","Grompe M","Kaestner KH","Luo Y","Streeter PR","Bramswig NC","Liu C","Dorrell C"],"additional_accession":[]},"is_claimable":false,"name":"Epigenomic plasticity enables human pancreatic α to β cell reprogramming.","description":"Insulin-secreting β cells and glucagon-secreting α cells maintain physiological blood glucose levels, and their malfunction drives diabetes development. Using ChIP sequencing and RNA sequencing analysis, we determined the epigenetic and transcriptional landscape of human pancreatic α, β, and exocrine cells. We found that, compared with exocrine and β cells, differentiated α cells exhibited many more genes bivalently marked by the activating H3K4me3 and repressing H3K27me3 histone modifications. This was particularly true for β cell signature genes involved in transcriptional regulation. Remarkably, thousands of these genes were in a monovalent state in β cells, carrying only the activating or repressing mark. Our epigenomic findings suggested that α to β cell reprogramming could be promote","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013 Mar","modification":"2025-04-25T22:00:15.843Z","creation":"2019-03-27T01:05:17Z"},"accession":"S-EPMC3582140","cross_references":{"pubmed":["23434589"],"doi":["10.1172/jci66514","10.1172/JCI66514"]}}