期刊
EMBO REPORTS
卷 10, 期 11, 页码 1242-1249出版社
WILEY
DOI: 10.1038/embor.2009.210
关键词
CagA; NF-kappa B; TAK1; TRAF6/ubiquitination
资金
- National Institutes of Health [DK-58587, CA-77955, CA-116087, AI45928]
- Robert A. Welch Foundation [E-1311]
Helicobacter pylori-initiated chronic gastritis is characterized by the cag pathogenicity island-dependent upregulation of proinflammatory cytokines, which is largely mediated by the transcription factor nuclear factor (NF)-kappa B. However, the cag pathogenicity island-encoded proteins and cellular signalling molecules that are involved in H. pylori-induced NF-kappa B activation and inflammatory response remain unclear. Here, we show that H. pylori virulence factor CagA and host protein transforming growth factor-beta-activated kinase 1 (TAK1) are essential for H. pylori-induced activation of NF-kappa B. CagA physically associates with TAK1 and enhances its activity and TAK1-induced NF-kappa B activation through the tumour necrosis factor receptor-associated factor 6-mediated, Lys 63-linked ubiquitination of TAK1. These findings show that polyubiquitination of TAK1 regulates the activation of NF-kappa B, which in turn is used by H. pylori CagA for the H. pylori-induced inflammatory response.
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