Abstract
Helicobacter pylori induces motogenic and cytoskeletal responses in gastric epithelial cells. We demonstrate that these responses can be induced via independent signaling pathways that often occur in parallel. The cag pathogenicity island appears to be nonessential for induction of motility, whereas the elongation phenotype depends on translocation and phosphorylation of CagA.
MeSH terms
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Antigens, Bacterial / genetics
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Antigens, Bacterial / metabolism
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Bacterial Proteins / genetics
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Bacterial Proteins / metabolism
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Cell Movement*
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Cells, Cultured
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Cytoskeleton / metabolism
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Epithelial Cells / microbiology*
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Epithelial Cells / ultrastructure
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Gastric Mucosa / cytology
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Gastric Mucosa / microbiology*
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Gene Expression Regulation, Bacterial
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Helicobacter pylori / genetics
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Helicobacter pylori / pathogenicity*
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Humans
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Signal Transduction*
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Transfection
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Virulence
Substances
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Antigens, Bacterial
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Bacterial Proteins
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cagA protein, Helicobacter pylori