<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/GSE309nnn/GSE309864/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Genomics</omics_type><species>Mus musculus</species><gds_type>Genome binding/occupancy profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE309864</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Modulating MyoD1 dosage activates alternate cell fate beyond myogenic differentiation [ATAC-seq]</name><description>The study investigates how MyoD1 dosage controls myogenic cell fate, employing bulk RNA-seq, ATAC-seq, and CUT&amp;RUN. We determined genome-wide transcriptional, chromatin accessibility, and MyoD1 binding profiles in C2C12 myoblasts expressing endogenous Halo-tagged MyoD1 or doxycycline-inducible Halo–MyoD1, under growth and differentiation conditions with low or high MyoD1 dosage.</description><dates><publication>2026/06/03</publication></dates><accession>GSE309864</accession><cross_references><GSM>GSM9283709</GSM><GSM>GSM9283708</GSM><GSM>GSM9283707</GSM><GSM>GSM9283706</GSM><GSM>GSM9283701</GSM><GSM>GSM9283700</GSM><GSM>GSM9283710</GSM><GSM>GSM9283699</GSM><GSM>GSM9283698</GSM><GSM>GSM9283705</GSM><GSM>GSM9283704</GSM><GSM>GSM9283703</GSM><GSM>GSM9283702</GSM><GSM>GSM9283697</GSM><GSM>GSM9283696</GSM><GSM>GSM9283695</GSM><GPL>24247</GPL><GSE>309864</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>