<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/GSE319663/</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=GSE319663</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>ChIP-seq analysis of HT-29 cells treated with the KDM5B inhibitors JB-157 or JB-161</name><description>KDM5B, a member of the KDM5 family of histone demethylases, functions as a key epigenetic regulator by removing di- and trimethyl groups from H3K4 (H3K4me2/3), thereby promoting transcriptional repression. It is involved in fundamental biological processes, including development, stem cell maintenance, and tumorigenesis, and its dysregulation has been associated with multiple cancer types. Given its critical role in cancer biology, KDM5B has emerged as an attractive target for therapeutic intervention. Therefore, we conducted a screening campaign to identify novel KDM5B inhibitors. In this study, we investigated whether the KDM5B inhibitors JB-157 and JB-161, identified through our screening, induce chromatin remodeling in HT-29 cells.</description><dates><publication>2026/07/01</publication></dates><accession>GSE319663</accession><cross_references><GSM>GSM9523142</GSM><GSM>GSM9523141</GSM><GSM>GSM9523143</GSM><GPL>34284</GPL><GSE>319663</GSE><taxon>Homo sapiens</taxon><PMID>[42324589]</PMID></cross_references></HashMap>