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Characterization of CagI in the Cag Pathogenicity Island of <Emphasis Type="Italic">Helicobacter pylori</Emphasis>
Authors:Hua?Wang  Jun?Han  Deyu?Chen  Xiujie?Duan  Xiaohuan?Gao  Xiaochun?Wang  Email author" target="_blank">Shihe?ShaoEmail author
Institution:(1) School of Medical Science and Laboratory Medicine, Jiangsu University, 301 Xuefu Road, Zhenjiang, 212013, Jiangsu, People’s Republic of China;(2) Department of Clinical Laboratory, Nanjing Children Hospital Affiliated to Nanjing Medical University, Nanjing, 210008, Jiangsu, China;(3) Department of Clinical Laboratory, Affiliated to Jiangsu University, Zhenjiang, 212011, Jiangsu, China;
Abstract:Helicobacter pylori is a highly successful human-specific gastric pathogen that infects up to 50% of the world’s population. Virulent H. pylori isolates harbor the cytotoxin-associated genes pathogenicity island (cag-PAI), which encodes a type IV secretion system that translocates bacterial effector (e.g., CagA oncoprotein) molecules into host cells. Although some cag-PAI genes are shown to be required for CagA delivery or localization, the majority have no known function. In the current study, the authors performed a cell components fractionation assay and showed that CagI, one of the cag-PAI proteins located in the bacterial membrane, was not translocated into host cells. The homologous recombination method then was used to construct the isogenic mutant of H. pylori cagI, and the translocation assay was performed. The results showed that the isogenic mutant of H. pylori NCTC 11637 cagI could cause a reduction in the degree of CagA translocation. Overall, the results suggested that CagI might be an accessory component of the CagA secretion system not translocated into host cells and that it is located in the bacterial membrane.
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