FIGURE 2.

BRG1 interacts with AP-1 to activate TBK1 transcription. (A) A TBK1 promoter-luciferase construct (–1,351/ + 76) was transfected into primary hepatocytes isolated from WT and BRG1^LKO mice followed by treatment with PA (0.4 mM). Luciferase activities were normalized by protein concentration and GFP fluorescence. (B) Primary hepatocytes were treated with PA (0.4 mM) and harvested at indicated time points. ChIP assay was performed with anti-BRG1 or IgG. (C) C57B6/L mice were fed an HFHC diet for 16 weeks. ChIP assay was performed with anti-BRG1 or IgG. (D) C57B6/L mice were fed an MCD diet for 8 weeks. ChIP assay was performed with anti-BRG1 or IgG. (E,F) Primary hepatocytes were transfected with indicated siRNAs followed by treatment with PA (0.4 mM) for 12 h. Knockdown efficiency was verified by Western blotting. ChIP assay was performed with anti-BRG1. (G) Wild type or mutant TBK1 promoter-luciferase construct was transfected into primary hepatocytes followed by treatment with PA (0.4 mM). Luciferase activities were normalized by protein concentration and GFP fluorescence. *p < 0.05 (one-way ANOVA with post hoc Scheffe test). Data are expressed as mean ± standard deviation (SD). All experiments were performed in triplicate wells and repeated three times. One representative experiment is shown.