{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE328nnn/GSE328411/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"scores":null,"additional":{"omics_type":["Genomics"],"species":["Homo sapiens"],"gds_type":["Genome binding/occupancy profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE328411"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"ChIP-seq of GLTSCR1 and SS18::SSX fusion in HS-SY-II synovial sarcoma cells treated with the BRD9 PROTAC degrader WA-68 across a time course","description":"Synovial sarcoma (SyS) is driven by the SS18::SSX fusion oncoprotein, which incorporates into GBAF chromatin remodeling complexes and creates a dependency on BRD9. To investigate the effects of BRD9 loss, we performed ChIP-seq, ATAC-seq, and RNA-seq in SyS models following BRD9 degradation. ChIP-seq shows reduced GBAF occupancy at target loci, while ATAC-seq reveals maintained or increased chromatin accessibility. RNA-seq demonstrates sustained or elevated expression of target genes. These results indicate that BRD9 is not required for GBAF assembly but instead restrains its remodeling activity, providing a mechanistic explanation for the limited efficacy of BRD9-targeted therapies in SyS.","dates":{"publication":"2026/06/24"},"accession":"GSE328411","cross_references":{"GSM":["GSM9682413","GSM9682402","GSM9682403","GSM9682411","GSM9682400","GSM9682401","GSM9682412","GSM9682410","GSM9682408","GSM9682409","GSM9682406","GSM9682407","GSM9682404","GSM9682405"],"GPL":["34281"],"GSE":["328411"],"taxon":["Homo sapiens"]}}