Regulation of RKIP Function by Helicobacter pylori in Gastric Cancer
Figure 4
The pathogenicity island of H. pylori is responsible for RKIP phosphorylation.
Western blot analysis of (A) AGS cells co-cultured with H. pylori strains for 6 h and examined for the indicated proteins. C = control (uninfected), WT = AGS cells infected with wild type H. pylori for 6 h, PAI- and oipA- represent isogenic mutants lacking these genes. (B) AGS cells transiently transfected for 24 h with RKIP S153 cDNA or 24 h and co-cultured with H. pylori for 6 h. (C) RKIP luciferase reporter assay of AGS cells transiently transfected with S153V RKIP in the presence or absence of H. pylori infection. In comparison to empty vector controls, the relative activity of RKIP transcription was increased by: *H. pylori, p<0.002; **RKIP, p<0.002; ***S153V, p<0.03, ****H. pylori and RKIP, p<0.0005; *****H. pylori and S153V, p<0.003. **, RKIP transcriptional activity was significantly decreased by the S153V compared with the wild type RKIP construct in response to H. pylori, #, p<0.0003. The data represents the mean +/− sd of 2 independent experiments performed in duplicate.