Fig. 6

BRG1-H3K14ac complex plays a crucial role in fibrotic responses, and MCL disrupts this complex. a–f BRG1 expression vector and H3K14 different mutation vectors were co-transfected into HMrSV5 cells. Lysine 14 was mutated into glutamine to mimic acetylation and mutated into arginine to inhibit acetylation, named as H3K14Q or H3K14R, respectively. Western blot analyses (a) and quantitative data of Fibronectin (b), Collagen I (c), P-Smad2 (d), H3K14ac (e) and TGF-β1 (f) in different groups are presented. *P < 0.05 versus vector, #P < 0.05 versus pBRG1. g Co-immunoprecipitation demonstrated that BRG1 interacted with H3K14ac in HMrSV5 cells, which was blocked by MCL. Cells were incubated with TGF-β1 with or with DMSO or different concentration of MCL for 48 h. Cell lysates were IP with anti-BRG1, followed by IB with anti-BRG1 and anti-H3K14ac