Encephalomyocarditis Virus 3C Protease relieves TANK Inhibitory Effect on TRAF6-mediated NF-kappaB S

• 作 者: LiHuang[1]QinfangLiu[1]LijieZhang[2]QuanZhang[2]LiangHu[1]ChangyaoLi[1]ShengnanWang[1]JiangnanLi[1]YuanfengZhang[1]HuibinYu[1]YanWang[3]ZhaohuaZhong[4]TaoXiong[5]XueshanXia[6]XiaojunWang[1]LiYu[1]Guoh
• 机 构: State Key Laboratory of Veterinary Biotechnology,Harbin Veterinary Research Institute of Chinese Aca
• 出 处: 中国畜牧兽医学会生物技术学分会暨中国免疫学会兽医免疫分会第十二次学术研讨会
• 发表日期: 2016年期

　　TRAF family member-associated NF-κB activator(TANK)is a negative regulator of canonical NF-κB signaling in the Toll-like receptor(TLR)-and B-cell receptor(BLR)-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(EMCV)3C at the 197 and 291 glutamine residues, which depends on its cysteine protease activity.In addition,EMCV 3C impaired the ability of TANK to inhibit TRAF6-mediated NF-κB signaling.Interestingly,we found that several viral proteases encoded by foot and mouth diseases virus(FMDV),porcine reproductive and respiratory syndrome virus(PRRSV)and equine arteritis virus(EAV)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.