promotes the oncogenic activity of CagA

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promotes the oncogenic activity of CagA Figure 1 Co-infection with Helicobacter pylori and EBV in gastric epithelial cells promotes the oncogenic activity of CagA Figure 1 | Co-infection with Helicobacter pylori and EBV in gastric epithelial cells promotes the oncogenic activity of CagA. CagA is translocated into host cells by the H. pylori cag secretion system where it is tyrosine phosphorylated by Src and Abl kinases. a | In the absence of Epstein–Barr virus (EBV), SHP1 interacts with CagA and negatively regulates CagA phosphorylation. b | With concomitant EBV infection, the SHP1 promoter is hypermethylated and its expression is downregulated. This process results in elevated levels of oncogenic phosphorylated CagA. Wroblewski, L. E. & Peek, R. M. Jr. (2016) Pathogenic enablers — toxic relationships in the stomach Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2016.68