<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/GSE250nnn/GSE250542/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</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=GSE250542</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Endogenous expression of inactive lysine deacetylases KDAC4 (HDAC4) and KDAC7 (HDAC7)</name><description>To investigate the roles of KDAC4 and KDAC7, we generated cell lines containing point mutations in HT1080 cells that result in endogenous expression of mutated proteins. For KDAC4, we introduced a mutation (H803A) to inactivate catalysis but that also contains concurrent mutations resulting in a knockout, as well as one that enhances in vitro activity of KDAC4 (H976Y, heterozygous with a knockout mutation on the second chromosal copy). For KDAC7, an inactivating mutation (H709A, homozygous) was introduced. Expression profiling analysis was then performed on the resulting cell lines and wild-type HT1080 cells treated with the KDAC inhibitor TMP195, vs. untreated wild-type HT1080.</description><dates><publication>2026/07/01</publication></dates><accession>GSE250542</accession><cross_references><GSM>GSM7981340</GSM><GSM>GSM7981341</GSM><GSM>GSM7981342</GSM><GSM>GSM7981343</GSM><GSM>GSM7981344</GSM><GSM>GSM7981334</GSM><GSM>GSM7981345</GSM><GSM>GSM7981346</GSM><GSM>GSM7981335</GSM><GSM>GSM7981336</GSM><GSM>GSM7981347</GSM><GSM>GSM7981348</GSM><GSM>GSM7981337</GSM><GSM>GSM7981338</GSM><GSM>GSM7981339</GSM><GPL>24676</GPL><GSE>250542</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>