乙型肝炎病毒 X 蛋白通过上调 TBK1 激活 NF-κB 信号通路。
The hepatitis B viral X protein activates NF-kappaB signaling pathway through the up-regulation of TBK1.
机构信息
The Department of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul, South Korea.
出版信息
FEBS Lett. 2010 Feb 5;584(3):525-30. doi: 10.1016/j.febslet.2009.11.091. Epub 2009 Dec 3.
The hepatitis B viral X protein (HBx) is a multifunctional protein that plays a role in the activation of the NF-kappaB signaling pathway. In this study, we demonstrate that HBx up-regulates expression of TANK-binding kinase-1 (TBK1) at the transcriptional level. Increased levels of TBK1 protein then induce the phosphorylation of NF-kappaB p65 at serine 536. Because TBK1 is up-regulated by HBx as part of its promotion of NF-kappaB activation, it is possible that increased TBK1 levels play a role in the development of hepatocellular carcinoma (HCC). From these data, we suggest that TBK1 may play a role in the HBx-mediated activation of the NF-kappaB signaling pathway and the development of HCCs.
乙型肝炎病毒 X 蛋白 (HBx) 是一种多功能蛋白，在 NF-κB 信号通路的激活中发挥作用。在这项研究中，我们证明 HBx 在转录水平上上调 TANK 结合激酶-1 (TBK1) 的表达。TBK1 蛋白水平的升高继而诱导 NF-κB p65 丝氨酸 536 的磷酸化。由于 TBK1 作为 HBx 促进 NF-κB 激活的一部分被上调，因此 TBK1 水平的升高可能在肝细胞癌 (HCC) 的发展中发挥作用。根据这些数据，我们认为 TBK1 可能在 HBx 介导的 NF-κB 信号通路激活和 HCC 的发展中发挥作用。
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