Helicobacter pylori stimulates epithelial cell migration via CagA-mediated perturbation of host cell signaling.
Microbes Infect
; 14(5): 470-6, 2012 May.
Article
en En
| MEDLINE
| ID: mdl-22202178
Helicobacter pylori CagA is delivered into gastric epithelial cells, where undergoes tyrosine phosphorylation at the Glu-Pro-Ile-Tyr-Ala (EPIYA) motif to interact with Src homology 2-containing protein tyrosine phosphatase-2 (SHP2) oncoprotein. CagA also binds to partitioning-defective 1 (PAR1) polarity-regulating kinase via the CagA multimerization (CM) sequence. To investigate pathophysiological role of CagA-SHP2 and/or CagA-PAR1 interaction in H. pylori infection, we generated H. pylori isogenic strains producing a phosphorylation-resistant CagA and a CagA without CM sequence. Infection studies revealed that deregulation of epithelial cell motility was more prominent in the wild-type strain than in the mutant strains. Thus, both CagA-SHP2 and CagA-PAR1 interactions are involved in the pathogenicity of cagA-positive H. pylori.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Proteínas Bacterianas
/
Transducción de Señal
/
Movimiento Celular
/
Helicobacter pylori
/
Factores de Virulencia
/
Células Epiteliales
/
Interacciones Huésped-Patógeno
/
Antígenos Bacterianos
Límite:
Humans
Idioma:
En
Revista:
Microbes Infect
Asunto de la revista:
ALERGIA E IMUNOLOGIA
/
MICROBIOLOGIA
Año:
2012
Tipo del documento:
Article
País de afiliación:
Japón
Pais de publicación:
Francia