{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T07:54:46Z","timestamp":1789372486824,"version":"build-2803163510"},"reference-count":50,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2001,12,21]],"date-time":"2001-12-21T00:00:00Z","timestamp":1008892800000},"content-version":"vor","delay-in-days":234,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Microbiology"],"published-print":{"date-parts":[[2001,5]]},"abstract":"<jats:p> <jats:italic>Helicobacter pylori<\/jats:italic> has been identified as the major aetiological agent in the development of chronic gastritis and duodenal ulcer, and it plays a role in the development of gastric carcinoma. Attachment of <jats:italic>H. pylori<\/jats:italic> to gastric epithelial cells leads to nuclear and cytoskeletal responses in host cells. Here, we show that Rho GTPases Rac1 and Cdc42 were activated during infection of gastric epithelial cells with either the wild\u2010type <jats:italic>H. pylori<\/jats:italic> or the mutant strain <jats:italic>cagA<\/jats:italic>. In contrast, no activation of Rho GTPases was observed when <jats:italic>H. pylori<\/jats:italic> mutant strains (<jats:italic>virB7<\/jats:italic> and PAI) were used that lack functional type IV secretion apparatus. We demonstrated that <jats:italic>H. pylori<\/jats:italic>\u2010induced activation of Rac1 and Cdc42 led to the activation of p21\u2010activated kinase 1 (PAK1) mediating nuclear responses, whereas the mutant strain PAI had no effect on PAK1 activity. Activation of Rac1, Cdc42 and PAK1 represented a very early event in colonization of gastric epithelial cells by <jats:italic>H. pylori<\/jats:italic>. Rac1 and Cdc42 were recruited to the sites of bacterial attachment and are therefore probably involved in the regulation of local and overall cytoskeleton rearrangement in host cells. Finally, actin rearrangement and epithelial cell motility in <jats:italic>H. pylori<\/jats:italic> infection depended on the presence of a functional type IV secretion system encoded by the <jats:italic>cag<\/jats:italic> pathogenicity island (PAI).<\/jats:p>","DOI":"10.1046\/j.1365-2958.2001.02443.x","type":"journal-article","created":{"date-parts":[[2003,3,12]],"date-time":"2003-03-12T11:37:10Z","timestamp":1047469030000},"page":"815-823","source":"Crossref","is-referenced-by-count":76,"title":["Pathogenicity island\u2010dependent activation of Rho GTPases Rac1 and Cdc42 in <i>Helicobacter pylori<\/i> infection"],"prefix":"10.1111","volume":"40","author":[{"given":"Yuri","family":"Churin","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Efterpi","family":"Kardalinou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas 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