GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE328nnn/GSE328410/primaryOK200GenomicsHomo sapiensGenome binding/occupancy profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE328410GEOGSEfalseATAC-seq of synovial sarcoma cell lines treated with the BRD9 PROTAC degrader WA-68Synovial 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.2026/06/24GSE328410GSM9682389GSM9682398GSM9682387GSM9682399GSM9682388GSM9682396GSM9682385GSM9682397GSM9682386GSM9682383GSM9682394GSM9682395GSM9682384GSM9682392GSM9682393GSM9682390GSM968239134281328410Homo sapiens