Fig. 5.

BRG1 interacts with AP-1 to activate CCL7 transcription in a redox-sensitive manner. (A) CCL7 promoter-luciferase constructs were transfected into HepG2 cells with or without BRG1 followed by treatment with LPS or PA. Luciferase activities were normalized by protein concentration and GFP fluorescence. (B) HepG2 cells were transfected with siRNA targeting AP-1 or scrambled siRNA (SCR) followed by treatment with LPS or PA. ChIP assays were performed with anti-BRG1 or IgG. (C) HepG2 cells were treated with LPS or PA in the presence or absence of NAC. ChIP assays were performed with anti-c-Jun, anti-c-Fos, or anti-BRG1. (D) HepG2 cells were treated with LPS or PA in the presence or absence of NAC. Immunoprecipitation was performed with anti-BRG1 or IgG. (E) C57/BL6 mice were injected with LPS in the presence or absence of NAC for 12 h. Immunoprecipitation was performed with anti-BRG1. (F) C57/BL6 mice were fed an MCD diet in the presence or absence of NAC for 4wk. Immunoprecipitation was performed with anti-BRG1. (G) HepG2 cells were treated with LPS or PA for 12 h. Re-ChIP assay was performed with indicated antibodies.