<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/GSE319nnn/GSE319426/</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=GSE319426</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Sodium Channel Isoform Diversity Underlies Chamber-Specific Cardiac Excitability [bulk RNA-seq]</name><description>Sodium channels are essential for cardiac conduction and excitability. The sodium current is primarily carried by the voltage gated sodium channel isoform NaV1.5. Using a novel NaV1.5 chimeric construct (NaV1.5-GX), our study reveals a unique chamber-specific distribution of non-NaV1.5 sodium channel isoforms, and we performed bulk RNA sequencing of murine ventricles to assess if acute NaV1.5 inhibition changed the trascriptional profile of the ventricular myocytes.</description><dates><publication>2026/04/09</publication></dates><accession>GSE319426</accession><cross_references><GSM>GSM9517837</GSM><GSM>GSM9517826</GSM><GSM>GSM9517825</GSM><GSM>GSM9517836</GSM><GSM>GSM9517828</GSM><GSM>GSM9517827</GSM><GSM>GSM9517829</GSM><GSM>GSM9517831</GSM><GSM>GSM9517830</GSM><GSM>GSM9517833</GSM><GSM>GSM9517832</GSM><GSM>GSM9517835</GSM><GSM>GSM9517824</GSM><GSM>GSM9517834</GSM><GPL>24247</GPL><GSE>319426</GSE><taxon>Mus musculus</taxon><PMID>[41878815]</PMID></cross_references></HashMap>