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U.S.A."],"published-print":{"date-parts":[[1997,7,8]]},"abstract":"<jats:p>\n                    Adherence of\n                    <jats:italic>Helicobacter pylori<\/jats:italic>\n                    to cultured gastric epithelial cells is associated with several cellular events, including the tyrosine phosphorylation of a 145-kDa host protein; the reorganization of the host cell actin and associated cellular proteins, like vasodilator-stimulated phosphoprotein, adjacent to the attached bacterial cell; and the subsequent release of the cytokine, interleukin 8 (IL-8).\n                    <jats:italic>H. pylori<\/jats:italic>\n                    isolated from patients with ulcer disease and gastric cancer contain a DNA insertion, the cag pathogenicity island (PAI), that is not present in bacteria isolated from individuals with asymptomatic infection. Mutations in a number of PAI genes abolish tyrosine phosphorylation and IL-8 synthesis but not the cytoskeletal rearrangements. Kinase inhibition studies suggest there are two distinct pathways operative in stimulating IL-8 release from host cells and one of these\n                    <jats:italic>H. pylori<\/jats:italic>\n                    pathways is independent of the tyrosine phosphorylation step.\n                  <\/jats:p>","DOI":"10.1073\/pnas.94.14.7595","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:31:44Z","timestamp":1027679504000},"page":"7595-7599","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":158,"title":["Induction of host signal transduction pathways by\n                    <i>Helicobacter\u2009pylori<\/i>"],"prefix":"10.1073","volume":"94","author":[{"given":"Ellyn D.","family":"Segal","sequence":"first","affiliation":[{"name":"Departments of Microbiology and Immunology and Medicine, and Digestive Disease Center, Stanford University School of Medicine, Stanford, CA 94305; Rocky Mountain Laboratory, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840; and Immunolbiological Research Institute, Siena, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C.","family":"Lange","sequence":"additional","affiliation":[{"name":"Departments of Microbiology and Immunology and Medicine, and Digestive Disease Center, Stanford University School of Medicine, Stanford, CA 94305; Rocky Mountain Laboratory, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840; and Immunolbiological Research Institute, Siena, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Covacci","sequence":"additional","affiliation":[{"name":"Departments of Microbiology and Immunology and Medicine, and Digestive Disease Center, Stanford University School of Medicine, Stanford, CA 94305; Rocky Mountain Laboratory, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840; and Immunolbiological Research Institute, Siena, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L. 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