<HashMap><database>GEO</database><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE297181</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Repression of Progenitor Programs Safeguards Pancreatic Endocrine Cell Identity</name><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.</description><dates><publication>2026/05/14</publication></dates><accession>GSE297181</accession><cross_references><GSM>GSM8985074</GSM><GSM>GSM8985075</GSM><GPL>24247</GPL><GSE>297181</GSE><taxon>Mus musculus</taxon><PMID>[41700921]</PMID></cross_references></HashMap>