Translocation of Helicobacter pylori CagA into Gastric Epithelial Cells by Type IV Secretion

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Science  25 Feb 2000:
Vol. 287, Issue 5457, pp. 1497-1500
DOI: 10.1126/science.287.5457.1497

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The Gram-negative bacterium Helicobacter pylori is a causative agent of gastritis and peptic ulcer disease in humans. Strains producing the CagA antigen (cagA +) induce strong gastric inflammation and are strongly associated with gastric adenocarcinoma and MALT lymphoma. We show here that such strains translocate the bacterial protein CagA into gastric epithelial cells by a type IV secretion system, encoded by the cagpathogenicity island. CagA is tyrosine-phosphorylated and induces changes in the tyrosine phosphorylation state of distinct cellular proteins. Modulation of host cells by bacterial protein translocation adds a new dimension to the chronicHelicobacter infection with yet unknown consequences.

  • * To whom correspondence should be addressed at Max von Pettenkofer Institute, Pettenkoferstrasse 9a, D-80336 Munich, Germany. E-mail: haas{at}

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