Fig. 4
From: SMARCA4 loss is synthetic lethal with CDK4/6 inhibition in non-small cell lung cancer
Extensive opening of regulatory elements by induction of SMARCA4/2. a Venn diagram showing overlap of open chromatin sites in control infected H1703 cells with or without SMARCA4 overexpression. Note the dramatic increase in open chromatin sites upon SMARCA4 overexpression. b Distribution of SMARCA4-dependent and -independent open chromatin sites relative to nearest gene transcriptional start site. Note that SMARCA4-dependent sites are much less likely to be promoters (within 1 kb of transcription start site (TSS)). c, d Metaplot (c) and heatmap (d) of assay for transposase-accessible chromatin sequencing (ATAC-seq) read data from control-infected, SMARCA4-infected and SMARCA2-infected cells over the 62,878 SMARCA4-dependent ATAC peaks. Note similar effect of SMARCA2 and SMARCA4. e, f Metaplot (e) and heatmap (f) of H3K27Ac chromatin immunoprecipitation (ChIP) data from control-transfected, SMARCA4-infected and SMARCA2-infected cells over the 62,878 SMARCA4-dependent ATAC peaks
