<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE324nnn/GSE324884/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><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=GSE324884</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>CBP/p300 deficiency induces the loss of functional pancreatic α cell mass</name><description>Pancreatic α cell senses amino acid availability to adjust secretion function and proliferation, yet the underlying molecular mechanisms remain unclear. Here, α cell-specific deletion of CBP/p300 in mice leads to hypoglucagonemia and hyperaminoacidemia, along with decreased functional pancreatic α cell mass due to impaired cell proliferation, dedifferentiation, and cell loss. The knockout of CBP/p300 blocks glucagon receptor antibody-stimulated α cell proliferation and mTORC1 signaling in mice. These findings uncover a critical role for CBP/p300 in the maintenance of α cell identity and function.</description><dates><publication>2026/06/18</publication></dates><accession>GSE324884</accession><cross_references><GSM>GSM9588302</GSM><GSM>GSM9588303</GSM><GPL>24247</GPL><GSE>324884</GSE><taxon>Mus musculus</taxon><PMID>[41965878]</PMID></cross_references></HashMap>