<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/GSE338nnn/GSE338699/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></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=GSE338699</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Helicobacter pylori infection-induced succinate accumulation drives IBS-D via KAT2A-mediated H3K79 succinylation</name><description>To explore the molecular mechanisms underlying Helicobacter pylori (Hp)-induced diarrhea-predominant irritable bowel syndrome (IBS-D), C57BL/6 mice were allocated into normal control (NC), Hp-infected, and succinate-treated (SA) groups. Alterations in colonic motility and visceral hypersensitivity were then assessed. Comparative RNA-sequencing (RNA-seq) of colonic tissues was performed to identify differentially expressed genes and elucidate the downstream molecular effectors mediating luminal succinate-driven dysmotility</description><dates><publication>2026/09/03</publication></dates><accession>GSE338699</accession><cross_references><GSM>GSM9880241</GSM><GSM>GSM9880240</GSM><GSM>GSM9880239</GSM><GSM>GSM9880238</GSM><GSM>GSM9880237</GSM><GSM>GSM9880236</GSM><GSM>GSM9880244</GSM><GSM>GSM9880243</GSM><GSM>GSM9880242</GSM><GPL>21103</GPL><GSE>338699</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>