Helicobacter pylori induces NF-kappaB independent of CagA.
作者信息
Schweitzer Katrin, Sokolova Olga, Bozko Przemyslaw M, Naumann Michael
出版信息
EMBO Rep. 2010 Jan;11(1):10-1; author reply 11-2. doi: 10.1038/embor.2009.263.
Abstract
摘要
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本文引用的文献
1
Helicobacter pylori CagA activates NF-kappaB by targeting TAK1 for TRAF6-mediated Lys 63 ubiquitination.幽门螺杆菌 CagA 通过靶向 TAK1 进行 TRAF6 介导的 Lys63 泛素化来激活 NF-κB。
EMBO Rep. 2009 Nov;10(11):1242-9. doi: 10.1038/embor.2009.210. Epub 2009 Oct 9.
2
Helicobacter pylori CagA phosphorylation-independent function in epithelial proliferation and inflammation.幽门螺杆菌CagA在上皮细胞增殖和炎症中的磷酸化非依赖性功能。
Cell Host Microbe. 2009 Jan 22;5(1):23-34. doi: 10.1016/j.chom.2008.11.010.
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Curcumin blocks NF-kappaB and the motogenic response in Helicobacter pylori-infected epithelial cells.姜黄素可阻断幽门螺杆菌感染的上皮细胞中的核因子-κB及促运动反应。
Biochem Biophys Res Commun. 2004 Apr 16;316(4):1065-72. doi: 10.1016/j.bbrc.2004.02.158.
4
Helicobacter pylori induces apoptosis of rat gastric parietal cells.幽门螺杆菌诱导大鼠胃壁细胞凋亡。
Am J Physiol Gastrointest Liver Physiol. 2002 Aug;283(2):G309-18. doi: 10.1152/ajpgi.00546.2001.
5
Systematic mutagenesis of the Helicobacter pylori cag pathogenicity island: essential genes for CagA translocation in host cells and induction of interleukin-8.幽门螺杆菌cag致病岛的系统诱变：宿主细胞中CagA易位及白细胞介素-8诱导的必需基因。
Mol Microbiol. 2001 Dec;42(5):1337-48. doi: 10.1046/j.1365-2958.2001.02714.x.
6
Activation of activator protein 1 and stress response kinases in epithelial cells colonized by Helicobacter pylori encoding the cag pathogenicity island.在编码cag致病岛的幽门螺杆菌定殖的上皮细胞中，激活蛋白1和应激反应激酶的激活。
J Biol Chem. 1999 Oct 29;274(44):31655-62. doi: 10.1074/jbc.274.44.31655.
7
cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors.cag是幽门螺杆菌的一个致病岛，编码I型特异性和疾病相关的毒力因子。
Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14648-53. doi: 10.1073/pnas.93.25.14648.
8
Interleukin-8 response of gastric epithelial cell lines to Helicobacter pylori stimulation in vitro.胃上皮细胞系对幽门螺杆菌体外刺激的白细胞介素-8反应
Infect Immun. 1995 May;63(5):1681-87. doi: 10.1128/iai.63.5.1681-1687.1995.
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