Helicobacter pylori VacA: a new perspective on an invasive chloride channel

被引：62

作者：

Rassow, Joachim ^{[1
]}

Meinecke, Michael ^{[2
,3
]}

机构：

[1] Ruhr Univ Bochum, Inst Physiol Chem, D-44780 Bochum, Germany

[2] Univ Gottingen, Biochem Abt 2, D-37073 Gottingen, Germany

[3] European Neurosci Inst Gottingen, D-37077 Gottingen, Germany

来源：

MICROBES AND INFECTION | 2012年 / 14卷 / 12期

关键词：

Helicobacter pylori; VacA; Mitochondria; Invasive ion channel; Reactive oxygen species; CYTOCHROME-C RELEASE; MITOCHONDRIAL PERMEABILITY TRANSITION; (ROS)-INDUCED ROS RELEASE; ANION-SELECTIVE CHANNELS; VACUOLATING CYTOTOXIN; BAX TRANSLOCATION; LIPID-BILAYERS; CELL-DEATH; TOXIN; AUTOPHAGY;

D O I：

10.1016/j.micinf.2012.07.002

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

The vacuolating cytotoxin VacA, a polypeptide of about 88 kDa, is one of the major virulence factors of Helicobacter pylori. VacA essentially acts as an invasive chloride channel targeting mitochondria. The results of recent studies open a new perspective on the mechanisms by which VacA causes loss of the mitochondrial membrane potential, mitochondrial fragmentation, formation of reactive oxygen species, autophagy, cell death and gastric cancer. (C) 2012 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.

引用

页码：1026 / 1033

页数：8

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