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


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 Cgamma 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 PLCgamma 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.

SUBMITTER: Churin Y 

PROVIDER: S-EPMC2172921 | biostudies-literature | 2003 Apr

REPOSITORIES: biostudies-literature

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

Churin Yuri Y   Al-Ghoul Laila L   Kepp Oliver O   Meyer Thomas F TF   Birchmeier Walter W   Naumann Michael M  

The Journal of cell biology 20030401 2


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 Cgamma  ...[more]

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