<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/GSE305nnn/GSE305453/</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=GSE305453</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>In vivo Perturb-seq uncovers key obstacles to heart repair and regeneration through direct reprogramming</name><description>We investigated the mechanism underlying Calr suppression-enhanced cardiac reprogramming. As CALR functions as an ER-resident chaperone and Ca2+-binding protein, with Ca2+ acting as a second messenger in fate-determining pathways, particularly cardiogenesis we performed RNA-seq on MGTMyoS-induced MICFs transduced with shCalr or shNT at days 7 and 14 in vitro</description><dates><publication>2026/03/21</publication></dates><accession>GSE305453</accession><cross_references><GSM>GSM9177278</GSM><GSM>GSM9177279</GSM><GSM>GSM9177276</GSM><GSM>GSM9177287</GSM><GSM>GSM9177277</GSM><GSM>GSM9177281</GSM><GSM>GSM9177282</GSM><GSM>GSM9177280</GSM><GSM>GSM9177285</GSM><GSM>GSM9177274</GSM><GSM>GSM9177275</GSM><GSM>GSM9177286</GSM><GSM>GSM9177283</GSM><GSM>GSM9177273</GSM><GSM>GSM9177284</GSM><GPL>24247</GPL><GSE>305453</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>