H. pylori mobilizes infected epithelial cells on its course to pathogenicity. The authors now show that mobilization results from activation of the hepatocyte growth factor (HGF) receptor c-Met. During development and differentiation, HGF-induced activation of c-Met initiates cell migration events. Inhibition of c-Met expression by siRNA blocks H. pylori–induced motility. H. pylori corrupts c-Met signaling, however, by injecting host cells with the protein CagA. Binding of CagA to c-Met resulted in modulation of receptor activity and recruitment of PLCγ, a mediator of cell polarity necessary for...
The Rockefeller University Press
2003
The Rockefeller University Press
2003
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