Infection and Immunity, June 2004, p. 3646-3649, Vol. 72, No. 6
0019-9567/04/$08.00+0 DOI: 10.1128/IAI.72.6.3646-3649.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Helicobacter pylori Induces AGS Cell Motility and Elongation via Independent Signaling Pathways
Stefan Moese,1 Matthias Selbach,1 Terry Kwok,2 Volker Brinkmann,3 Wolfgang König,2 Thomas F. Meyer,1 and Steffen Backert2*
Department of Molecular Biology,1
Microscopy Unit, Max Planck Institute for Infection Biology, D-10117 Berlin,3
Department of Medical Microbiology, Otto von Guericke University, D-39120 Magdeburg, Germany2
Received 15 December 2003/
Returned for modification 12 January 2004/
Accepted 2 March 2004
Helicobacter pylori induces motogenic and cytoskeletal responses in gastric epithelial cells. We demonstrate that these responses can be induced via independent signaling pathways that often occur in parallel. The cag pathogenicity island appears to be nonessential for induction of motility, whereas the elongation phenotype depends on translocation and phosphorylation of CagA.
* Corresponding author. Mailing address: Otto von Guericke University, Dept. of Medical Microbiology, Leipziger Str. 44, D-39120 Magdeburg, Germany. Phone: 49 0391-67 13329. Fax: 49 0391-67 190469. E-mail: Steffen.Backert{at}medizin.uni-magdeburg.de.
Editor: D. L. Burns
Infection and Immunity, June 2004, p. 3646-3649, Vol. 72, No. 6
0019-9567/04/$08.00+0 DOI: 10.1128/IAI.72.6.3646-3649.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
This article has been cited by other articles:
-
Snider, J. L., Allison, C., Bellaire, B. H., Ferrero, R. L., Cardelli, J. A.
(2008). The {beta}1 Integrin Activates JNK Independent of CagA, and JNK Activation Is Required for Helicobacter pylori CagA+-induced Motility of Gastric Cancer Cells. J. Biol. Chem.
283: 13952-13963
[Abstract]
[Full Text]
-
Bourzac, K. M., Botham, C. M., Guillemin, K.
(2007). Helicobacter pylori CagA Induces AGS Cell Elongation through a Cell Retraction Defect That Is Independent of Cdc42, Rac1, and Arp2/3. Infect. Immun.
75: 1203-1213
[Abstract]
[Full Text]
-
Andrzejewska, J., Lee, S. K., Olbermann, P., Lotzing, N., Katzowitsch, E., Linz, B., Achtman, M., Kado, C. I., Suerbaum, S., Josenhans, C.
(2006). Characterization of the Pilin Ortholog of the Helicobacter pylori Type IV cag Pathogenicity Apparatus, a Surface-Associated Protein Expressed during Infection.. J. Bacteriol.
188: 5865-5877
[Abstract]
[Full Text]
-
Kusters, J. G., van Vliet, A. H. M., Kuipers, E. J.
(2006). Pathogenesis of Helicobacter pylori Infection. Clin. Microbiol. Rev.
19: 449-490
[Abstract]
[Full Text]
-
Pinto-Santini, D., Salama, N. R.
(2005). The Biology of Helicobacter pylori Infection, a Major Risk Factor for Gastric Adenocarcinoma. Cancer Epidemiol. Biomarkers Prev.
14: 1853-1858
[Abstract]
[Full Text]
Copyright © 2004 by the American Society for Microbiology. All rights reserved.