<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/GSE317nnn/GSE317978/</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=GSE317978</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>The role of BAF60C in type 2 diabetes——RNAseq</name><description>This research identify reduced expression of BAF60C in diabetic islets and demonstrate that altered β-cell BAF60C levels strongly influence metabolic homeostasis. Genetic loss of BAF60C in β-cells exacerbates hyperglycemia and islet dysfunction under metabolic stress, whereas β-cell–specific restoration of BAF60C produces protective effects. These findings establish BAF60C as an important regulator of β-cell integrity and disease progression in T2D.</description><dates><publication>2026/02/06</publication></dates><accession>GSE317978</accession><cross_references><GSM>GSM9483790</GSM><GSM>GSM9483796</GSM><GSM>GSM9483795</GSM><GSM>GSM9483798</GSM><GSM>GSM9483797</GSM><GSM>GSM9483792</GSM><GSM>GSM9483791</GSM><GSM>GSM9483794</GSM><GSM>GSM9483793</GSM><GSM>GSM9483804</GSM><GSM>GSM9483803</GSM><GSM>GSM9483806</GSM><GSM>GSM9483805</GSM><GSM>GSM9483800</GSM><GSM>GSM9483789</GSM><GSM>GSM9483788</GSM><GSM>GSM9483802</GSM><GSM>GSM9483801</GSM><GSM>GSM9483807</GSM><GSM>GSM9483785</GSM><GSM>GSM9483784</GSM><GSM>GSM9483787</GSM><GSM>GSM9483786</GSM><GSM>GSM9483783</GSM><GSM>GSM9483799</GSM><GPL>23479</GPL><GSE>317978</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>