The Helicobacter pylori CagA protein disrupts matrix adhesion of gastric epithelial cells by dephosphorylation of vinculin
β Scribed by Stefan Moese; Matthias Selbach; Volker Brinkmann; Alexander Karlas; Beatrice Haimovich; Steffen Backert; Thomas F. Meyer
- Book ID
- 109041442
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 865 KB
- Volume
- 9
- Category
- Article
- ISSN
- 1462-5814
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## Abstract Infection with CagAβpositive __Helicobacter pylori__ is the strongest risk factor for gastric carcinoma. Upon delivery into gastric epithelial cells, CagA disturbs cellular functions by physically interacting with and deregulating intracellular signaling molecules via both tyrosine phos
## Abstract In this study, we have evaluated the effects on cell cycle regulation of VacA alone and in combination with other two __Helicobacter pylori__ proteins, cytotoxinβassociated protein (CagA) and HspB, using the human gastric epithelial cells (AGS). Our results indicate that VacA alone was