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本文引用的文献

1
Phosphorylation of tyrosine 972 of the Helicobacter pylori CagA protein is essential for induction of a scattering phenotype in gastric epithelial cells.幽门螺杆菌CagA蛋白酪氨酸972位点的磷酸化对于诱导胃上皮细胞的散射表型至关重要。
Mol Microbiol. 2001 Nov;42(3):631-44. doi: 10.1046/j.1365-2958.2001.02649.x.
2
Identification of a tyrosine-phosphorylated 35 kDa carboxy-terminal fragment (p35CagA) of the Helicobacter pylori CagA protein in phagocytic cells: processing or breakage?在吞噬细胞中鉴定幽门螺杆菌CagA蛋白的酪氨酸磷酸化35 kDa羧基末端片段（p35CagA）：是加工还是断裂？
Proteomics. 2001 Apr;1(4):618-29. doi: 10.1002/1615-9861(200104)1:4<618::AID-PROT618>3.0.CO;2-C.
3
Tyrosine phosphorylation patterns and size modification of the Helicobacter pylori CagA protein after translocation into gastric epithelial cells.幽门螺杆菌CagA蛋白转位至胃上皮细胞后的酪氨酸磷酸化模式及大小修饰
Proteomics. 2001 Apr;1(4):608-17. doi: 10.1002/1615-9861(200104)1:4<608::AID-PROT608>3.0.CO;2-G.
4
Pathogenicity island-dependent activation of Rho GTPases Rac1 and Cdc42 in Helicobacter pylori infection.幽门螺杆菌感染中致病性岛依赖性的Rho GTP酶Rac1和Cdc42激活
Mol Microbiol. 2001 May;40(4):815-23. doi: 10.1046/j.1365-2958.2001.02443.x.
5
Living dangerously: how Helicobacter pylori survives in the human stomach.险境求生：幽门螺杆菌如何在人类胃部存活。
Nat Rev Mol Cell Biol. 2001 Jun;2(6):457-66. doi: 10.1038/35073084.
6
Role of Helicobacter pylori cag region genes in colonization and gastritis in two animal models.幽门螺杆菌cag区域基因在两种动物模型的定植和胃炎中的作用。
Infect Immun. 2001 May;69(5):2902-8. doi: 10.1128/IAI.69.5.2902-2908.2001.
7
Interaction of Helicobacter pylori with professional phagocytes: role of the cag pathogenicity island and translocation, phosphorylation and processing of CagA.幽门螺杆菌与专职吞噬细胞的相互作用：cag致病岛的作用以及CagA的转位、磷酸化和加工
Cell Microbiol. 2001 Jan;3(1):21-31. doi: 10.1046/j.1462-5822.2001.00088.x.
8
Translocation of the Helicobacter pylori CagA protein in gastric epithelial cells by a type IV secretion apparatus.幽门螺杆菌CagA蛋白通过IV型分泌系统在胃上皮细胞中的易位。
Cell Microbiol. 2000 Apr;2(2):155-64. doi: 10.1046/j.1462-5822.2000.00043.x.
9
implication of the structure of the Helicobacter pylori cag pathogenicity island in induction of interleukin-8 secretion.幽门螺杆菌cag致病岛结构在诱导白细胞介素-8分泌中的作用
Infect Immun. 2001 Mar;69(3):1625-9. doi: 10.1128/IAI.69.3.1625-1629.2001.
10
Crystal structure of the hexameric traffic ATPase of the Helicobacter pylori type IV secretion system.幽门螺杆菌IV型分泌系统六聚体转运ATP酶的晶体结构
Mol Cell. 2000 Dec;6(6):1461-72. doi: 10.1016/s1097-2765(00)00142-8.

幽门螺杆菌cag致病岛的功能分析揭示了VirD4-CagA依赖性和VirD4-CagA非依赖性机制。

Functional analysis of the Helicobacter pylori cag pathogenicity island reveals both VirD4-CagA-dependent and VirD4-CagA-independent mechanisms.

作者信息

Selbach Matthias, Moese Stefan, Meyer Thomas F, Backert Steffen

机构信息

Abteilung Molekulare Biologie, Max-Planck-Institut für Infektionsbiologie, D-10117 Berlin, Germany.

出版信息

Infect Immun. 2002 Feb;70(2):665-71. doi: 10.1128/IAI.70.2.665-671.2002.

DOI:10.1128/IAI.70.2.665-671.2002
PMID:11796597
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC127714/
Abstract

The type IV secretion machinery encoded by the cag pathogenicity island (PAI) of Helicobacter pylori has been implicated in a series of host responses during infection. Here, we analyzed the function of 12 cag PAI genes from both cag I and cag II loci, including the complete virB/D complex (virB4, virB7, virB8, virB9, virB10, virB11, and virD4). We monitored interleukin-8 (IL-8) secretion, CagA translocation and tyrosine phosphorylation, and induction of a scattering ("hummingbird") phenotype upon H. pylori infection of AGS gastric epithelial cells. For the first time, we have complemented individual cag PAI gene knockout mutants with their intact genes expressed from a shuttle vector and showed that complemented CagA and VirD4 restored wild-type function. Our results demonstrate that phenotypic changes and phosphorylation of CagA depended on all virB/D genes and several other genes of the cag PAI. Induction of IL-8 secretion depended largely on the same set of genes but was independent of CagA and VirD4. Thus, CagA translocation and induction of IL-8 secretion are regulated by VirD4-CagA-dependent and VirD4-CagA-independent mechanisms, respectively. The function of VirD4 as a possible adapter protein which guides CagA into the type IV secretion channel is presented in a model.

摘要

幽门螺杆菌cag致病岛（PAI）编码的IV型分泌机制与感染期间的一系列宿主反应有关。在此，我们分析了来自cag I和cag II位点的12个cag PAI基因的功能，包括完整的virB/D复合体（virB4、virB7、virB8、virB9、virB10、virB11和virD4）。我们监测了白细胞介素-8（IL-8）分泌、CagA易位和酪氨酸磷酸化，以及幽门螺杆菌感染AGS胃上皮细胞后诱导的散射（“蜂鸟”）表型。我们首次用穿梭载体表达的完整基因对单个cag PAI基因敲除突变体进行了互补，并表明互补后的CagA和VirD4恢复了野生型功能。我们的结果表明，CagA的表型变化和磷酸化依赖于所有virB/D基因和cag PAI的其他几个基因。IL-8分泌的诱导很大程度上依赖于同一组基因，但独立于CagA和VirD4。因此，CagA易位和IL-8分泌的诱导分别由VirD4-CagA依赖性和VirD4-CagA非依赖性机制调节。在一个模型中展示了VirD4作为一种可能的衔接蛋白将CagA引导到IV型分泌通道的功能。