GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE328nnn/GSE328411/primary200OKGenomicsHomo sapiensGenome binding/occupancy profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE328411GEOGSEfalseChIP-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 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.2026/06/24GSE328411GSM9682413GSM9682402GSM9682403GSM9682411GSM9682400GSM9682401GSM9682412GSM9682410GSM9682408GSM9682409GSM9682406GSM9682407GSM9682404GSM968240534281328411Homo sapiens