首页> 美国卫生研究院文献>The Journal of Biological Chemistry >Encephalomyocarditis Virus 3C Protease Relieves TRAF Family Member-associated NF-κB Activator (TANK) Inhibitory Effect on TRAF6-mediated NF-κB Signaling through Cleavage of TANK
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Encephalomyocarditis Virus 3C Protease Relieves TRAF Family Member-associated NF-κB Activator (TANK) Inhibitory Effect on TRAF6-mediated NF-κB Signaling through Cleavage of TANK

机译:脑心肌炎病毒3C蛋白酶通过切割TANK减轻TRAF家族成员相关的NF-κB激活剂(TANK)对TRAF6介导的NF-κB信号的抑制作用。

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摘要

TRAF family member-associated NF-κB activator (TANK) is a negative regulator of canonical NF-κB signaling in the Toll-like receptor- and B-cell receptor-mediated signaling pathways. However, functions of TANK in viral infection-mediated NF-κB activation remain unclear. Here, we reported that TANK was cleaved by encephalomyocarditis virus 3C at the 197 and 291 glutamine residues, which depends on its cysteine protease activity. In addition, encephalomyocarditis virus 3C impaired the ability of TANK to inhibit TRAF6-mediated NF-κB signaling. Interestingly, we found that several viral proteases encoded by the foot and mouth disease virus, porcine reproductive and respiratory syndrome virus, and equine arteritis virus also cleaved TANK. Our results suggest that TANK is a novel target of some viral proteases, indicating that some positive RNA viruses have evolved to utilize their major proteases to regulate NF-κB activation.
机译:TRAF家族成员相关的NF-κB激活剂(TANK)是Toll样受体和B细胞受体介导的信号通路中经典NF-κB信号的负调节剂。但是,TANK在病毒感染介导的NF-κB活化中的功能仍不清楚。在这里,我们报道了TANK被脑心肌炎病毒3C在197和291个谷氨酰胺残基处裂解,这取决于其半胱氨酸蛋白酶的活性。此外,脑心肌炎病毒3C损害了TANK抑制TRAF6介导的NF-κB信号传导的能力。有趣的是,我们发现口蹄疫病毒,猪繁殖与呼吸综合征病毒和马动脉炎病毒编码的几种病毒蛋白酶也能裂解TANK。我们的结果表明,TANK是某些病毒蛋白酶的新靶标,表明某些阳性RNA病毒已进化为利用其主要蛋白酶来调节NF-κB的活化。

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