Abstract
Helicobacter pylori virulence factor CagA is injected into gastric epithelial cells and undergoes tyrosine phosphorylation. Similar to mammalian Gab protein, tyrosine-phosphorylated CagA recruits and activates SHP-2 phosphatase at the plasma membrane, thereby inducing a growth factor-like effect. CagA-SHP-2 interaction may play an important role in bacterial pathogenesis, leading to gastric carcinoma.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Antigens, Bacterial / metabolism*
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Bacterial Proteins / metabolism*
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Epithelial Cells / microbiology
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Epithelial Cells / pathology
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Gastric Mucosa / microbiology
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Gastric Mucosa / physiopathology
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Helicobacter Infections / microbiology
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Helicobacter Infections / physiopathology
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Helicobacter pylori / pathogenicity*
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Humans
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Intracellular Signaling Peptides and Proteins
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Phosphoproteins / metabolism*
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Protein Tyrosine Phosphatase, Non-Receptor Type 11
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Protein Tyrosine Phosphatases / metabolism*
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Signal Transduction
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Stomach Neoplasms / microbiology*
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Stomach Neoplasms / physiopathology
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Virulence
Substances
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Antigens, Bacterial
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Bacterial Proteins
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Intracellular Signaling Peptides and Proteins
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Phosphoproteins
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cagA protein, Helicobacter pylori
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PTPN11 protein, human
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Protein Tyrosine Phosphatase, Non-Receptor Type 11
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Protein Tyrosine Phosphatases