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Helicobacter pylori CagA protein targets the c-Met receptor and enhances the motogenic response

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Item Type:Article
Title:Helicobacter pylori CagA protein targets the c-Met receptor and enhances the motogenic response
Creators Name:Churin, Y. and Al Ghoul, L. and Kepp, O. and Meyer, T.E. and Birchmeier, W. and Naumann, M.
Abstract:Infection with the human microbial pathogen Helicobacter pylori is assumed to lead to invasive gastric cancer. We find that H. pylori activates the hepatocyte growth factor/scatter factor receptor c-Met, which is involved in invasive growth of tumor cells. The H. pylori effector protein CagA intracellularly targets the c-Met receptor and promotes cellular processes leading to a forceful motogenic response. CagA could represent a bacterial adaptor protein that associates with phospholipase C{gamma} but not Grb2-associated binder 1 or growth factor receptor-bound protein 2. The H. pylori-induced motogenic response is suppressed and blocked by the inhibition of PLC{gamma} and of MAPK, respectively. Thus, upon translocation, CagA modulates cellular functions by deregulating c-Met receptor signaling. The activation of the motogenic response in H. pylori-infected epithelial cells suggests that CagA could be involved in tumor progression.
Keywords:Epithelial-Mesenchymal Transition, Hepatocyte Growth Factor, Motility, Tumor Invasion, Motogenic Response, PLC{gamma}
Source:Journal of Cell Biology
Publisher:Rockefeller University Press (U.S.A.)
Page Range:249-255
Date:28 April 2003
Additional Information:Copyright (c) 2003 by The Rockefeller University Press
Official Publication:https://doi.org/10.1083/jcb.200208039
PubMed:View item in PubMed

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