<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/GSE311nnn/GSE311116/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Genomics</omics_type><species>Homo sapiens</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=GSE311116</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>DDIT4 overexpression reshapes the histone modification landscape in human coronary artery smooth muscle cells: an H3K9ac and H3K27ac CUT&amp;Tag study</name><description>This study investigates the epigenetic mechanisms by which DDIT4 promotes vascular smooth muscle cell (VSMC) dedifferentiation. We performed CUT&amp;Tag sequencing for the active histone marks H3K9ac and H3K27ac in HCASMCs following DDIT4 overexpression. Our findings reveal that DDIT4, by inhibiting the pyruvate dehydrogenase complex, reduces acetyl-CoA levels and globally decreases histone acetylation. Specifically, we observe loss of H3K9ac and H3K27ac at the promoters of key contractile genes, providing an epigenetic explanation for the DDIT4-mediated suppression of the contractile phenotype and acceleration of atherosclerosis.</description><dates><publication>2026/06/06</publication></dates><accession>GSE311116</accession><cross_references><GSM>GSM9317297</GSM><GSM>GSM9317296</GSM><GSM>GSM9317295</GSM><GSM>GSM9317294</GSM><GSM>GSM9317293</GSM><GSM>GSM9317292</GSM><GSM>GSM9317291</GSM><GSM>GSM9317290</GSM><GSM>GSM9317289</GSM><GSM>GSM9317300</GSM><GSM>GSM9317299</GSM><GSM>GSM9317298</GSM><GPL>34284</GPL><GSE>311116</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>