<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/GSE318nnn/GSE318796/</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=GSE318796</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>RNA-seq analysis of B16F10 cells following p300/CBO knockout</name><description>The p300 and CBP (CREB-binding protein) paralogs are essential histone acetyltransferases (HATs) that serve as global transcriptional coactivators. In many cancers, including melanoma, these proteins redundantly regulate key oncogenic and lineage-specific gene programs. To investigate their combined role in melanoma, we generated p300/CBP sinlge and double-knockout (dKO) B16F10 murine melanoma cells using CRISPR/Cas9. We then performed bulk RNA-sequencing to identify genes and biological pathways that are critically dependent on these coactivators. Our results define the shared and unique transcriptional targets of p300/CBP in the B16F10 model and provide a resource for understanding how their loss impacts melanoma cell fitness, invasive potential, and stress responses.</description><dates><publication>2026/04/29</publication></dates><accession>GSE318796</accession><cross_references><GSM>GSM9503416</GSM><GSM>GSM9503415</GSM><GSM>GSM9503418</GSM><GSM>GSM9503417</GSM><GSM>GSM9503419</GSM><GSM>GSM9503421</GSM><GSM>GSM9503420</GSM><GSM>GSM9503423</GSM><GSM>GSM9503412</GSM><GSM>GSM9503422</GSM><GSM>GSM9503414</GSM><GSM>GSM9503413</GSM><GPL>24247</GPL><GSE>318796</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>