JCB logo
R&D Systems: New Poster Available
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published 28 April 2003. doi:10.1083/jcb.200208039
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 282K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Churin, Y.
Right arrow Articles by Naumann, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Churin, Y.
Right arrow Articles by Naumann, M.
Right arrowPubmed/NCBI databases
*Substance via MeSH
Medline Plus Health Information
*Stomach Cancer
Related Collections
Right arrowRelated Article
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

© The Rockefeller University Press, 0021-9525/2003/4/249 $5.00
The Journal of Cell Biology, Volume 161, Number 2, 249-255

Report

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



Yuri Churin1, Laila Al-Ghoul2, Oliver Kepp1, Thomas F. Meyer1, Walter Birchmeier3 and Michael Naumann2

1 Department of Molecular Biology, Max Planck Institute for Infection Biology, 10117 Berlin, Germany
2 Institute of Experimental Internal Medicine, Medical Faculty, Otto-von-Guericke-University, 39120 Magdeburg, Germany
3 Max Delbrück Center for Molecular Medicine, 13092 Berlin, Germany

Address correspondence to Michael Naumann, Institute of Experimental Internal Medicine, Medical Faculty, Otto-von-Guericke-University, Leipziger Strasse 44, 39120 Magdeburg, Germany. Tel.: 49-391-67-13227. Fax: 49-391-67-190160. E-mail: naumann{at}medizin.uni-magdeburg.de

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.

Key Words: epithelial–mesenchymal transition; hepatocyte growth factor; motility; tumor invasion; motogenic response; PLC{gamma}

* Abbreviations used in this paper: EGFR, EGF receptor; ERK, extracellular-regulated kinase; HGF, hepatocyte growth factor; PAI, pathogenicity island; PI3-K, phosphatidylinositol 3-OH kinase; PKB, protein kinase B; PLC{gamma}, phospholipase C{gamma}; siRNA, small interfering RNA.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

Related Article

H. pylori mobilizes cells
Nicole LeBrasseur
J. Cell Biol. 2003 161: 219. [Full Text] [PDF]



This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents