幽门螺杆菌细胞毒素相关基因致病岛
The Helicobacter pylori cag Pathogenicity Island.
作者信息
Noto Jennifer M, Peek Richard M
机构信息
Division of Gastroenterology, Department of Medicine, Vanderbilt University Medical Center, MRB IV 1030C MRB IV, Nashville, TN, USA.
出版信息
Methods Mol Biol. 2012;921:41-50. doi: 10.1007/978-1-62703-005-2_7.
Abstract
The cag pathogenicity island is a well-characterized virulence determinant. It is composed of 32 genes that encode a type IV bacterial secretion system and is linked with a more severe clinical outcome. The following chapters will explore the manipulation of bacterial factors in order to understand their role in gastric mucosal disease.
摘要
cag致病岛是一种特征明确的毒力决定因素。它由32个基因组成，这些基因编码一种IV型细菌分泌系统，并且与更严重的临床结果相关。以下各章将探讨对细菌因素的操控，以便了解它们在胃黏膜疾病中的作用。
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本文引用的文献
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NOD1 contributes to mouse host defense against Helicobacter pylori via induction of type I IFN and activation of the ISGF3 signaling pathway.NOD1 通过诱导 I 型 IFN 和激活 ISGF3 信号通路促进小鼠宿主抵抗幽门螺杆菌。
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Helicobacter pylori induces MAPK phosphorylation and AP-1 activation via a NOD1-dependent mechanism.幽门螺杆菌通过 NOD1 依赖性机制诱导 MAPK 磷酸化和 AP-1 激活。
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Helicobacter pylori type IV secretion apparatus exploits beta1 integrin in a novel RGD-independent manner.幽门螺杆菌 IV 型分泌装置以一种新型的非 RGDI 依赖性方式利用β1 整合素。
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Helicobacter pylori CagA inhibits PAR1-MARK family kinases by mimicking host substrates.幽门螺杆菌 CagA 通过模拟宿主底物来抑制 PAR1-MARK 家族激酶。
Nat Struct Mol Biol. 2010 Jan;17(1):130-2. doi: 10.1038/nsmb.1705. Epub 2009 Dec 6.
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Bacterial membrane vesicles deliver peptidoglycan to NOD1 in epithelial cells.细菌膜泡将肽聚糖递呈给上皮细胞中的 NOD1。
Cell Microbiol. 2010 Mar;12(3):372-85. doi: 10.1111/j.1462-5822.2009.01404.x. Epub 2009 Nov 2.
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Mol Cell Proteomics. 2009 Aug;8(8):1947-58. doi: 10.1074/mcp.M900139-MCP200. Epub 2009 May 25.
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