Helicobacter pylori induces AGS cell motility and elongation via independent signaling pathways

Moese S, Selbach M, Kwok T, Brinkmann V, König W, Meyer TF, Backert S (2004)

Publication Type: Journal article

Publication year: 2004

Journal

Infection and Immunity American Society for Microbiology

Book Volume: 72

Pages Range: 3646-3649

Journal Issue: 6

DOI: 10.1128/IAI.72.6.3646-3649.2004

Abstract

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.

Authors with CRIS profile

Steffen Backert

Involved external institutions

Max-Planck-Institut für Infektionsbiologie / Max Planck Institute for Infection Biology DE Germany (DE) Otto-von-Guericke-Universität Magdeburg DE Germany (DE)

How to cite

APA:

Moese, S., Selbach, M., Kwok, T., Brinkmann, V., König, W., Meyer, T.F., & Backert, S. (2004). Helicobacter pylori induces AGS cell motility and elongation via independent signaling pathways. Infection and Immunity, 72(6), 3646-3649. https://doi.org/10.1128/IAI.72.6.3646-3649.2004

MLA:

Moese, Stefan, et al. "Helicobacter pylori induces AGS cell motility and elongation via independent signaling pathways." Infection and Immunity 72.6 (2004): 3646-3649.

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