CagA tyrosine phosphorylation and interleukin-8 induction by Helicobacter pylori are independent from AlpAB, HopZ and Bab group outer membrane proteins
- 1 January 2002
- journal article
- Published by Elsevier in International Journal of Medical Microbiology
- Vol. 292 (3-4) , 257-266
- https://doi.org/10.1078/1438-4221-00205
Abstract
No abstract availableKeywords
Funding Information
- Deutsche Forschungsgemeinschaft (HA 2697-5-3)
This publication has 50 references indexed in Scilit:
- The Evaluation of Putative Virulence Factors ofHelicobacter pylorifor Gastroduodenal Disease by Use of a Short‐Term Mongolian Gerbil Infection ModelThe Journal of Infectious Diseases, 2002
- Polymorphisms of Helicobacter pylori HP0638 Reflect Geographic Origin and Correlate with cagA StatusJournal of Clinical Microbiology, 2002
- Phosphorylation of tyrosine 972 of the Helicobacter pylori CagA protein is essential for induction of a scattering phenotype in gastric epithelial cellsMolecular Microbiology, 2001
- Comparative Genomics ofHelicobacter pylori: Analysis of the Outer Membrane Protein FamiliesInfection and Immunity, 2000
- Translocation of the Helicobacter pylori CagA protein in gastric epithelial cells by a type IV secretion apparatusCellular Microbiology, 2000
- Helicobacter pylori Caga Protein Can Be Tyrosine Phosphorylated in Gastric Epithelial CellsThe Journal of Experimental Medicine, 2000
- cag , a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factorsProceedings of the National Academy of Sciences, 1996
- The Bacteria Behind UlcersScientific American, 1996
- Attachment of Helicobacter pylori to Human Gastric Epithelium Mediated by Blood Group AntigensScience, 1993
- Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminoglycan heparan sulphateJournal of Medical Microbiology, 1993