Fig. 2: USP7 KO selectively impairs the super-enhancer of SMAD3.
From: USP7 facilitates SMAD3 autoregulation to repress cancer progression in p53-deficient lung cancer
A Venn diagram summarizing the H3K27ac ChIP-seq peaks identified in wildtype (WT, overlapped peaks of two biological repeats) and USP7 KO (overlapped peaks of two independent clones HKO_E2 and HKO_E3) H1299 cells. B Gene ontology (GO) biological terms of USP7 WT- and KO-specific H3K27ac ChIP-seq peaks in (A) using GREAT analysis. C H3K27ac loading across the enhancers in USP7 WT (left) and KO (right, clone HKO_E2) H1299 cell lines. Super-enhancers (SE) were identified using the ROSE program with default parameters. Numbers of identified SE are indicated at right. The SE-associated genes involved in the TGFβ-signal pathway were denoted. D The plot showing the fold changes of H3K27ac ChIP-seq signals for all identified SEs in H1299 cell lines. E IGV gene tracks of H3K27ac ChIP-seq signals in USP7 WT (two biological repeats) and KO (HKO_E2 and HKO_E3) H1299 cell lines at SMAD3 locus. Identified SE domains (right, SMAD3-SE1; left, SMAD3-SE2) are yellow-colored and indicated at the top.
