Regulation of the actin cytoskeleton in Helicobacter pylori-induced migration and invasive growth of gastric epithelial cells
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* Corresponding author: Silja Wessler silja.wessler@sbg.ac.at
1 Division of Molecular Biology, Department of Microbiology, University of Salzburg, Salzburg, Austria
2 University Clinic for Blood Group Serology and Transfusion Medicine, PMU, General Hospital Salzburg, SALK, Salzburg, Austria
Cell Communication and Signaling 2011, 9:27 doi:10.1186/1478-811X-9-27
Published: 1 November 2011Abstract
Dynamic rearrangement of the actin cytoskeleton is a significant hallmark of Helicobacter pylori (H. pylori) infected gastric epithelial cells leading to cell migration and invasive growth. Considering the cellular mechanisms, the type IV secretion system (T4SS) and the effector protein cytotoxin-associated gene A (CagA) of H. pylori are well-studied initiators of distinct signal transduction pathways in host cells targeting kinases, adaptor proteins, GTPases, actin binding and other proteins involved in the regulation of the actin lattice. In this review, we summarize recent findings of how H. pylori functionally interacts with the complex signaling network that controls the actin cytoskeleton of motile and invasive gastric epithelial cells.