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ATAC-seq analysis of NCI-H1693 cells treated with the selective SMARCA2 degrader PRT3789

ABSTRACT: The goal of this study was to characterize genome-wide chromatin accessibility changes induced by SMARCA2 degradation in a SMARCA4-deficient non-small cell lung cancer model. NCI-H1693 cells were treated with the selective SMARCA2 degrader PRT3789 (50 nM) or vehicle control (DMSO) for 48 h. ATAC-seq was performed to identify regions of differential accessibility that may help explain the mechanism of synthetic lethality in SMARCA4-deficient contexts.

ORGANISM(S): Homo sapiens

PROVIDER: GSE307426 | GEO | 2025/09/12

REPOSITORIES: GEO

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