Fig. 2. Silencing of KDM4B reduced the JNK/c-Jun and ERK signaling.

a Micro-Western Array heat-map chart shows the abundance and phosphorylation signal protein fold change of non-infected or H. pylori-infected sh4B#1 cells as compared to pLKO control cells. β-Actin was the internal control. b The expression of c-Jun and phosphorylation of c-Jun in non-infected or H. pylori-infected pLKO, sh4B#1, and sh4B#2 cells were detected by immunoblotting. c AGS cells were untreated or treated with SP600125 (25 μM) in the absence (−Hp) or presence of H. pylori (+ Hp) at an moi of 50 for 6 h. c-Jun, p-c-Jun, and β-actin were detected by immunoblotting. d IL-8 mRNA levels were measured from AGS cells untreated or treated with SP600125 according to (c). e AGS cells were treated with indicated concentrations of SP600125, followed by immunoblotting analysis with anti-KDM4B, anti-p-c-Jun, anti-c-Jun, and β-actin antibodies, respectively. *p < 0.05; **p < 0.01