{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE328nnn/GSE328410/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"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=GSE328410"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"ATAC-seq of synovial sarcoma cell lines treated with the BRD9 PROTAC degrader WA-68","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":"GSE328410","cross_references":{"GSM":["GSM9682389","GSM9682398","GSM9682387","GSM9682399","GSM9682388","GSM9682396","GSM9682385","GSM9682397","GSM9682386","GSM9682383","GSM9682394","GSM9682395","GSM9682384","GSM9682392","GSM9682393","GSM9682390","GSM9682391"],"GPL":["34281"],"GSE":["328410"],"taxon":["Homo sapiens"]}}