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Terry Kwok

Researcher at Monash University, Clayton campus

Publications -  45
Citations -  8048

Terry Kwok is an academic researcher from Monash University, Clayton campus. The author has contributed to research in topics: CagA & Helicobacter pylori. The author has an hindex of 21, co-authored 41 publications receiving 7331 citations. Previous affiliations of Terry Kwok include Florey Institute of Neuroscience and Mental Health & Otto-von-Guericke University Magdeburg.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Helicobacter exploits integrin for type IV secretion and kinase activation

TL;DR: It is shown that the H. pylori CagL protein is a specialized adhesin that is targeted to the pilus surface, where it binds to and activates integrin α5β1 receptor on gastric epithelial cells through an arginine-glycine-aspartate motif.
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NF-κB activation and potentiation of proinflammatory responses by the Helicobacter pylori CagA protein

TL;DR: The results suggest that IL-8 release induced by CagA occurs via a Ras-->Raf-->Mek-->Erk-->NF-kappaB signaling pathway in a Shp-2- and c-Met-independent manner, and is a multifunctional protein capable of effecting both actin remodeling and potentiation of chemokine release.
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Vacuolating cytotoxin A (VacA), a key toxin for Helicobacter pylori pathogenesis

TL;DR: This review summarizes and consolidates the recent advances in VacA toxin research, with focus on the outstanding controversies in the field and the key remaining questions that need to be addressed.
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Specific entry of Helicobacter pylori into cultured gastric epithelial cells via a zipper-like mechanism.

TL;DR: It is demonstrated that the entry of H. pylori into AGS cells occurs via a zipper-like mechanism which involves various host signal transduction events.