Role of HP1076 in Type IV secretion pathway of H. pylori
Invited conference paper presented and published in conference proceedings


摘要Introduction: Helicobacter pylori infection is recognized as a primary risk factor for gastric adenocarcinoma and gastric lymphoma. Strains of H. pylori harboring cag pathogenicity island are typically associated with higher rate of disease. Cag PAI encodes components of a type IV secretion system and an effector molecule CagA. Translocation of CagA by T4SS directly into gastric epithelial cells disturbs various major cellular functions that promotes gastric carcinogenesis. However, little is known about the T4SS in H. pylori.
Objectives: This study aims to investigate the functional significance of a hypothetical protein HP1076 by a combination of genetics and biochemical approaches.
Major findings: We show that release of CagA from H. pylori into gastric epithelial cells is reduced in HP1076-null strain. Intriguingly, interruption of HP1076 also leads to suppression of CagA phosphorylation. We further characterize the role of HP0176 in the assembly of T4SS and identify its potential interacting partners related to the modulation of CagA.
Conclusion/Implications: Our results suggest that HP1076 plays a critical role in T4SS and CagA secretion and modification. Given our increased understanding that CagA is closely associated with H. pylori pathogenesis, knowledge of this important export machinery and its mediated translocation of CagA will offer a blueprint for future studies of host-pathogen interaction.  
著者LAM Wai Ling, AU Shannon Wing Ngor
會議名稱25th FAOBMB Conference
會議論文集題名25th FAOBMB Conference

上次更新時間 2018-21-01 於 07:30