GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE328nnn/GSE328412/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE328412GEOGSEfalseRNA-seq of HS-SY-II synovial sarcoma cells treated with the BRD9 PROTAC degrader WA-68 across a time courseSynovial 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.2026/06/24GSE328412GSM9682414GSM9682422GSM9682423GSM9682420GSM9682421GSM9682419GSM9682417GSM9682418GSM9682415GSM968241634281328412Homo sapiens