{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE297nnn/GSE297181/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE297181"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Repression of Progenitor Programs Safeguards Pancreatic Endocrine Cell Identity","description":"Pancreatic endocrine cells regulate glucose homeostasis and energy metabolism in response to nutrients. All pancreatic endocrine cells originate from a common progenitor population through multiple coordinated cell fate decisions. ISL1 is a key lineage-determining transcription factor, but its role in endocrine cell identity, differentiation, and maturation is insufficiently characterized. By integrating single-cell RNA profiling with H3K27ac and H3K27me3 histone modification analyses, we identified a reshaped transcriptome and epigenetic landscape in Isl1-deficient endocrine cells leading to altered α-cell identity, loss of δ- and γ-cell lineages, and incompletely differentiated, immature β cells. We show that ISL1 represses intermediate developmental programs during endocrine cell differentiation and facilitates chromatin transitions to drive terminal differentiation and maturation. These findings provide insights into how combinatorial transcription factor-epigenome interactions activate and repress transcriptional programs driving cell fate acquisition, differentiation, and maturation during endocrine pancreas development.","dates":{"publication":"2026/05/14"},"accession":"GSE297181","cross_references":{"GSM":["GSM8985074","GSM8985075"],"GPL":["24247"],"GSE":["297181"],"taxon":["Mus musculus"],"PMID":["[41700921]"]}}