Oncogenic mechanisms of the Helicobacter pylori CagA protein (Q28280246)

Helicobacter pylori infectious disease

Europe PubMed Central

title

Oncogenic mechanisms of the Helicobacter pylori CagA protein (English)

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main subject

Helicobacter pylori

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Masanori Hatakeyama

1

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language of work or name

English

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publication date

September 2004

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published in

Nature Reviews Cancer

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volume

4

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issue

9

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page(s)

688-94

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cites work

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cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors

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Risk for gastric cancer in people with CagA positive or CagA negative Helicobacter pylori infection

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Helicobacter pylori CagA protein can be tyrosine phosphorylated in gastric epithelial cells

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Tyrosine phosphorylation of the Helicobacter pylori CagA antigen after cag-driven host cell translocation

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Translocation of Helicobacter pylori CagA into gastric epithelial cells by type IV secretion

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c-Src/Lyn kinases activate Helicobacter pylori CagA through tyrosine phosphorylation of the EPIYA motifs

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Src is the kinase of the Helicobacter pylori CagA protein in vitro and in vivo.

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SHP-2 tyrosine phosphatase as an intracellular target of Helicobacter pylori CagA protein

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Biological activity of the Helicobacter pylori virulence factor CagA is determined by variation in the tyrosine phosphorylation sites

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Phosphorylation of tyrosine 972 of the Helicobacter pylori CagA protein is essential for induction of a scattering phenotype in gastric epithelial cells

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Phosphotyrosine phosphatases with SH2 domains: regulators of signal transduction

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Genetic analysis of protein tyrosine phosphatases

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Protein-tyrosine phosphatase Shp-2 regulates cell spreading, migration, and focal adhesion

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Concerted activity of tyrosine phosphatase SHP-2 and focal adhesion kinase in regulation of cell motility

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The tyrosine phosphatase SHP-2 is required for sustained activation of extracellular signal-regulated kinase and epithelial morphogenesis downstream from the met receptor tyrosine kinase

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Somatic mutations in PTPN11 in juvenile myelomonocytic leukemia, myelodysplastic syndromes and acute myeloid leukemia

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Mutations in PTPN11 implicate the SHP-2 phosphatase in leukemogenesis

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Helicobacter pylori CagA induces Ras-independent morphogenetic response through SHP-2 recruitment and activation

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Attenuation of Helicobacter pylori CagA x SHP-2 signaling by interaction between CagA and C-terminal Src kinase

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The Helicobacter pylori CagA protein induces cortactin dephosphorylation and actin rearrangement by c-Src inactivation

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Suppression of Ras-induced apoptosis by the Rac GTPase

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A model for gastric cancer epidemiology

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The CagA protein of Helicobacter pylori is translocated into epithelial cells and binds to SHP-2 in human gastric mucosa

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SH2 domains from suppressor of cytokine signaling-3 and protein tyrosine phosphatase SHP-2 have similar binding specificities

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Gastric cancer development in mice lacking the SHP2 binding site on the IL-6 family co-receptor gp130.

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Grb2 is a key mediator of helicobacter pylori CagA protein activities

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Helicobacter pylori CagA protein targets the c-Met receptor and enhances the motogenic response

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Disruption of the epithelial apical-junctional complex by Helicobacter pylori CagA.

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Enteropathogenic E. coli Tir binds Nck to initiate actin pedestal formation in host cells

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Conditional gene silencing utilizing the lac repressor reveals a role of SHP-2 in cagA-positive Helicobacter pylori pathogenicity

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Relation between Helicobacter pylori cagA status and risk of peptic ulcer disease

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Increased risk of noncardia gastric cancer associated with proinflammatory cytokine gene polymorphisms

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Relationship between the cagA 3' repeat region of Helicobacter pylori, gastric histology, and susceptibility to low pH

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Characterization of and human serologic response to proteins in Helicobacter pylori broth culture supernatants with vacuolizing cytotoxin activity

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