<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/GSE189nnn/GSE189489/</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=GSE189489</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>RNAseq data of mouse B16-F10 melanoma cell lines after siEzh2 knockdown or GSK126 methyl-transferase inhibitor or DZNep treatment</name><description>Enhancer of zeste homolog 2 (EZH2) plays critical roles in the progression of many malignancies including melanoma. The most well-known EZH2 mechanism is regulating gene expression through catalysing tri-methylation of histone H3 at Lys 27 (H3K27me3). However, EZH2 also have methylation-independent activities that limit the therapeutic potential of EZH2 methyl-transferase inhibitors. To investigate the methyl-transferase independent role of EZH2 in melanoma, we performed global gene expression analysis of B16-F10 cells treated with methyl-transferase inhibitor GSK126 or siEzh2 knockdown or the EZH2 degrader DZNep.</description><dates><publication>2026/07/02</publication></dates><accession>GSE189489</accession><cross_references><GSM>GSM5702493</GSM><GSM>GSM5702492</GSM><GSM>GSM5702495</GSM><GSM>GSM5702484</GSM><GSM>GSM5702494</GSM><GSM>GSM5702486</GSM><GSM>GSM5702485</GSM><GSM>GSM5702488</GSM><GSM>GSM5702487</GSM><GSM>GSM5702491</GSM><GSM>GSM5702490</GSM><GSM>GSM5726839</GSM><GSM>GSM5726838</GSM><GSM>GSM5726837</GSM><GSM>GSM5702489</GSM><GPL>13112</GPL><SRA>SRP347616</SRA><GSE>189489</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>