Abstract
Infection with strains of Helicobacter pylori that carry the cytotoxin-associated antigen A (cagA) gene is associated with gastric carcinoma. Recent studies have shed light on the mechanism through which the cagA gene product, CagA, elicits pathophysiological actions. CagA is delivered into gastric epithelial cells by the bacterial type IV secretion system, where it deregulates the SHP2 oncoprotein. Intriguingly, CagA is noted for its variation, particularly at the SHP2-binding site, which could affect the potential of different strains of H. pylori to promote gastric carcinogenesis.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Antigens, Bacterial / metabolism
-
Antigens, Bacterial / pharmacology*
-
Bacterial Proteins / metabolism
-
Bacterial Proteins / pharmacokinetics
-
Bacterial Proteins / pharmacology*
-
Carcinoma / etiology*
-
Carcinoma / microbiology*
-
Cell Transformation, Neoplastic*
-
Down-Regulation
-
Helicobacter Infections / complications*
-
Helicobacter pylori / pathogenicity*
-
Humans
-
Intracellular Signaling Peptides and Proteins
-
Phosphorylation
-
Protein Tyrosine Phosphatase, Non-Receptor Type 11
-
Protein Tyrosine Phosphatases / metabolism*
-
Protein Tyrosine Phosphatases / pharmacology
-
SH2 Domain-Containing Protein Tyrosine Phosphatases
-
Stomach Neoplasms / etiology*
-
Stomach Neoplasms / microbiology*
-
src Homology Domains
Substances
-
Antigens, Bacterial
-
Bacterial Proteins
-
Intracellular Signaling Peptides and Proteins
-
cagA protein, Helicobacter pylori
-
PTPN11 protein, human
-
Protein Tyrosine Phosphatase, Non-Receptor Type 11
-
Protein Tyrosine Phosphatases
-
SH2 Domain-Containing Protein Tyrosine Phosphatases