Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. STKE, 29 March 2005
Vol. 2005, Issue 277, p. pe14
[DOI: 10.1126/stke.2772005pe14]


Orchestration of Aberrant Epithelial Signaling by Helicobacter pylori CagA

Richard M. Peek Jr.1*

1Division of Gastroenterology, Departments of Medicine and Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN 37232-2279, USA; Department of Veterans Affairs Medical Center, Nashville, TN 37212-2637, USA.

Abstract: Persistent colonization by Helicobacter pylori is the strongest risk factor for distal gastric adenocarcinoma, and H. pylori strains that harbor the cag pathogenicity island further augment cancer risk. The H. pylori cag island encodes a secretion system, and the product of the terminal gene in the island (CagA) is translocated into host epithelial cells after bacterial attachment, where it undergoes tyrosine phosphorylation by Src kinases and binds the eukaryotic phosphatase SHP-2. Higashi et al. now demonstrate that CagA-dependent SHP-2 activation leads to sustained activation of ERK (extracellular signal-regulated kinase), culminating in morphological changes that mimic unrestrained stimulation by growth factors. These data implicate the cag island as a key mediator of pathogenic epithelial responses that may heighten the risk for gastric cancer.

*Contact information. Telephone: (615) 322-5200; Fax: (615) 343-6229; e-mail: richard.peek{at}

Citation: R. M. Peek, Jr., Orchestration of Aberrant Epithelial Signaling by Helicobacter pylori CagA. Sci. STKE 2005, pe14 (2005).

Read the Full Text

Helicobacter and Salmonella Persistent Infection Strategies.
D. M. Monack (2013)
Cold Spring Harb Perspect Med 3, a010348
   Abstract »    Full Text »    PDF »
Mammalian Pragmin regulates Src family kinases via the Glu-Pro-Ile-Tyr-Ala (EPIYA) motif that is exploited by bacterial effectors.
F. Safari, N. Murata-Kamiya, Y. Saito, and M. Hatakeyama (2011)
PNAS 108, 14938-14943
   Abstract »    Full Text »    PDF »
Host-Interactive Genes in Amerindian Helicobacter pylori Diverge from Their Old World Homologs and Mediate Inflammatory Responses.
S. P. Mane, M. G. Dominguez-Bello, M. J. Blaser, B. W. Sobral, R. Hontecillas, J. Skoneczka, S. K. Mohapatra, O. R. Crasta, C. Evans, T. Modise, et al. (2010)
J. Bacteriol. 192, 3078-3092
   Abstract »    Full Text »    PDF »
Helicobacter pylori CagA activates NF-{kappa}B by targeting TAK1 for TRAF6-mediated Lys 63 ubiquitination.
A. Lamb, X.-D. Yang, Y.-H. N. Tsang, J.-D. Li, H. Higashi, M. Hatakeyama, R. M. Peek, S. R. Blanke, and L.-F. Chen (2009)
EMBO Rep. 10, 1242-1249
   Abstract »    Full Text »    PDF »

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882