Tegtmeyer N, Harrer A, Schmitt V, Singer BB, Backert S (2019)
Publication Type: Journal article
Publication year: 2019
Book Volume: 21
Article Number: e12965
Journal Issue: 1
DOI: 10.1111/cmi.12965
Helicobacter pylori represents an important pathogen involved in diseases ranging from gastritis, peptic ulceration, to gastric malignancies. Prominent virulence factors comprise the vacuolating cytotoxin VacA and the cytotoxin-associated genes pathogenicity island (cagPAI)-encoded type IV secretion system (T4SS). The T4SS effector protein CagA can be translocated into AGS and other gastric epithelial cells followed by phosphorylation through c-Src and c-Abl tyrosin kinases to hijack signalling networks. The duodenal cell line AZ-521 has been recently introduced as novel model system to investigate CagA delivery and phosphorylation in a VacA-dependent fashion. In contrast, we discovered that AZ-521 cells display a T4SS incompetence phenotype for CagA injection, which represents the first reported gastrointestinal cell line with a remarkable T4SS defect. We proposed that this deficiency may be due to an imbalanced coexpression of T4SS receptor integrin-β
APA:
Tegtmeyer, N., Harrer, A., Schmitt, V., Singer, B.B., & Backert, S. (2019). Expression of CEACAM1 or CEACAM5 in AZ-521 cells restores the type IV secretion deficiency for translocation of CagA by Helicobacter pylori. Cellular Microbiology, 21(1). https://dx.doi.org/10.1111/cmi.12965
MLA:
Tegtmeyer, Nicole, et al. "Expression of CEACAM1 or CEACAM5 in AZ-521 cells restores the type IV secretion deficiency for translocation of CagA by Helicobacter pylori." Cellular Microbiology 21.1 (2019).
BibTeX: Download