Fig. 6.

CK2-mediated BRG1 phosphorylation promotes its interaction with AP-1. (A, B) C57/BL6 mice were injected with LPS in the presence or absence of NAC for 12 h. CK2 expression levels in the liver were examined by qPCR and Western. Immunoprecipitation was performed with anti-BRG1. (C, D) C57/BL6 mice were fed an MCD diet in the presence or absence of NAC for 4wk. CK2 expression levels in the liver were examined by qPCR and Western. Immunoprecipitation was performed with anti-BRG1. (E) HepG2 cells were treated with LPS or PA in the presence or absence of NAC. CK2 expression levels were examined by qPCR. (F) Primary murine hepatocytes were treated with LPS or PA in the presence or absence of NAC. CK2 expression levels were examined by qPCR. (G) HepG2 cells were transfected with siRNA targeting CK2 or scrambled siRNA (SCR) followed by treatment with LPS or PA. Immunoprecipitation was performed with anti-BRG1. (H) HepG2 cells were transfected with siRNA targeting CK2 or scrambled siRNA (SCR) followed by treatment with LPS or PA. ChIP assay was performed with anti-BRG1. (I) HepG2 cells were transfected with siRNA targeting CK2 or scrambled siRNA (SCR) followed by treatment with LPS or PA. Re-ChIP assay was performed with indicated antibodies. (J-L) HepG2 cells were transfected with siRNA targeting CK2 or scrambled siRNA (SCR) followed by treatment with LPS or PA. CCL7 expression was examined by qPCR and ELISA. Conditioned media were collected and chemotaxis assay was performed as described in Methods.