A Helicobacter pylori Vacuolating Toxin Mutant That Fails To Oligomerize Has a Dominant Negative Phenotype

No abstract is available for this paper.

• Publication year

  2006

• Venue

  Infection and Immunity

• Publication date

  2006-03-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1128/IAI.74.3.1786-1794.2006PMID 16495552PMCID PMC1418680
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Helicobacter pylori toxin VacA is transferred to host cells via a novel contact‐dependent mechanism

  2004cited by this paper
• Inhibition of primary human T cell proliferation by Helicobacter pylori vacuolating toxin (VacA) is independent of VacA effects on IL-2 secretion.

  2004cited by this paper
• Interactions between p-33 and p-55 Domains of the Helicobacter pylori Vacuolating Cytotoxin (VacA)*

  2004cited by this paper
• Helicobacter pylori vacuolating cytotoxin enters cells, localizes to the mitochondria, and induces mitochondrial membrane permeability changes correlated to toxin channel activity

  2004cited by this paper
• The Helicobacter pylori Vacuolating Toxin Inhibits T Cell Activation by Two Independent Mechanisms

  2003cited by this paper
• Essential Role of a GXXXG Motif for Membrane Channel Formation by Helicobacter pylori Vacuolating Toxin*

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• Induction of gastric epithelial cell apoptosis by Helicobacter pylori vacuolating cytotoxin.

  2003cited by this paper
• Helicobacter pylori Vacuolating Cytotoxin Inhibits T Lymphocyte Activation

  2003cited by this paper
• Mice deficient in protein tyrosine phosphatase receptor type Z are resistant to gastric ulcer induction by VacA of Helicobacter pylori

  2003cited by this paper
• Cellular Vacuolation and Mitochondrial Cytochrome c Release Are Independent Outcomes of Helicobacter pylori Vacuolating Cytotoxin Activity That Are Each Dependent on Membrane Channel Formation*

  2003cited by this paper
• New insights into the molecular basis of progressive myoclonus epilepsy: a multiprotein complex with cystatin B.

  2002cited by this paper
• Multiple oligomeric states of the Helicobacter pylori vacuolating toxin demonstrated by cryo-electron microscopy.

  2002cited by this paper
• Key importance of the Helicobacter pylori adherence factor blood group antigen binding adhesin during chronic gastric inflammation.

  2001cited by this paper
• Vacuolating Cytotoxin of Helicobacter pylori Plays a Role during Colonization in a Mouse Model of Infection

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• Cellular Uptake of Clostridium botulinum C2 Toxin Requires Oligomerization and Acidification*

  2000cited by this paper
• Membrane topology of VacA cytotoxin from H. pylori

  2000cited by this paper
• High cell sensitivity to Helicobacter pylori VacA toxin depends on a GPI-anchored protein and is not blocked by inhibition of the clathrin-mediated pathway of endocytosis.

  2000cited by this paper
• Acid activation of Helicobacter pylori vacuolating cytotoxin (VacA) results in toxin internalization by eukaryotic cells

  2000cited by this paper
• The N‐terminal 34 kDa fragment of Helicobacter pylori vacuolating cytotoxin targets mitochondria and induces cytochrome c release

  2000cited by this paper
• A Dominant Negative Mutant of Helicobacter pyloriVacuolating Toxin (VacA) Inhibits VacA-induced Cell Vacuolation*

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• Clinical Pathogenesis, Molecular Mechanisms of Gastric Cancer Development.

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