ArticleCellular microbiology2008
OipA plays a role in Helicobacter pylori-induced focal adhesion kinase activation and cytoskeletal re-organization.
Article in Cellular microbiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
38 citing papers in PubMed, 68 citations in OpenAlex.
- Developing a potent vaccine againstExpert reviews in molecular medicine · 2024Review
- Pivotal role ofFrontiers in medicine · 2024Review
- How Long Will It Take to Launch an EffectiveInfection and drug resistance · 2023Review
- Host Cell Antimicrobial Responses againstInternational journal of molecular sciences · 2022Review
- Biomarker Characterization and Prediction of Virulence and Antibiotic Resistance fromBiomolecules · 2022Review
- Evaluation ofIranian journal of basic medical sciences · 2021Article
- Manipulation of Focal Adhesion Signaling by Pathogenic Microbes.International journal of molecular sciences · 2021Review
- Virulence of Helicobacter pylori outer membrane proteins: an updated review.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2020Review
- The Role ofGalen medical journal · 2020Article
- Tyrosine Kinases inToxins · 2019Review
- Rapid Characterization of Virulence Determinants inJournal of clinical medicine · 2019Article
- Genetic populations and virulence factors of Helicobacter pylori.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2018Review
- Attaching-and-Effacing Pathogens Exploit Junction Regulatory Activities of N-WASP and SNX9 to Disrupt the Intestinal Barrier.Cellular and molecular gastroenterology and hepatology · 2018Article
- Phosphorylation of phosphatase and tensin homolog induced byOncology letters · 2018Article
- Vibrio vulnificus MARTX cytotoxin causes inactivation of phagocytosis-related signaling molecules in macrophages.Journal of biomedical science · 2017Article
- Binding of the Helicobacter pylori OipA causes apoptosis of host cells via modulation of Bax/Bcl-2 levels.Scientific reports · 2017Article
- Review
- Gene polymorphisms of pathogenicWorld journal of gastroenterology · 2016Review
- What exists beyond cagA and vacA? Helicobacter pylori genes in gastric diseases.World journal of gastroenterology · 2015Review
- Effect of Helicobacter pylori Infection on the Composition of Gastric Microbiota in the Development of Gastric Cancer.Gastrointestinal tumors · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The initial signalling events leading to Helicobacter pylori infection associated changes in motility, cytoskeletal reorganization and elongation of gastric epithelial cells remain poorly understood. Because focal adhesion kinase (FAK) is known to play important roles in regulating actin cytoskeletal organization and cell motility we examined the effect of H. pylori in gastric epithelial cells co-cultured with H. pylori or its isogenic cag pathogenicity island (PAI) or oipA mutants. H. pylori induced FAK phosphorylation at distinct tyrosine residues in a dose- and time-dependent manner. Autophosphorylation of FAK Y397 was followed by phosphorylation of Src Y418 and resulted in phosphorylation of the five remaining FAK tyrosine sites. Phosphorylated FAK and Src activated Erk and induced actin stress fibre formation. FAK knock-down by FAK-siRNA inhibited H. pylori-mediated Erk phosphorylation and abolished stress fibre formation. Infection with oipA mutants reduced phosphorylation of Y397, Y576, Y577, Y861 and Y925, inhibited stress fibre formation and altered cell morphology. cag PAI mutants reduced phosphorylation of only FAK Y407 and had less effect on stress fibre formation than oipA mutants. We propose that activation of FAK and Src are responsible for H. pylori-induced induction of signalling pathways resulting in the changes in cell phenotype important for pathogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.