Helicobacter pylori is a gram-negative bacterium thought to be a primary cause of gastric ulcers and cancer. Within its arsenal, the CagA and VacA proteins bind host PTPs, and these events are critical for its detrimental effects. CagA is injected into host cells and perturbs cellular functions, including the induction of morphological changes. One target of CagA has been identified as SHP-2, and disruption of this complex abolishes the effects of CagA (Higashi et al. 2002). Hence, the formation of this complex also stimulates the phosphatase activity of SHP-2. On the other hand, VacA is critical for causing massive vacuolization of the host cell, and recently this process has been shown to be dependent on its ability to bind the receptor phospha-tase PTP-Z in a ligand-like fashion (Fujikawa et al. 2003).
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