Differential regulation of ERK1/2 activity in response to stimulation with HGF and H. pylori infection. a) MDCK cells were infected with H. pylori or stimulated with HGF as indicated, or left untreated. Total cell lysates were subjected to SDS-PAGE and immunoblotted. The basal level of ERK was used as load control. b) MDCK epithelial cells were pretreated with pharmacological inhibitors of PI3K (LY294002), MEK (PD98059) or PLCγ1 (U73122) and infected with H. pylori or activated by HGF. The basal level of ERK was used as load control. Western blot analysis shows that inhibition of PI3K has no effect on ERK1/2 activation. Treatment of the cells with MEK inhibitor blocks ERK1/2 activation by H. pylori and HGF. Inhibition of PLCγ1 blocks ERK1/2 activation in H. pylori transfected cells, but not in HGF activated cells.