Encephalomyocarditis Virus 3C Protease relieves TANK Inhibitory Effect on TRAF6-mediated NF-kappaB Signaling through Cleavage of TANK
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- 英文论文题名：Encephalomyocarditis Virus 3C Protease relieves TANK Inhibitory Effect on TRAF6-mediated NF-kappaB Signaling through Cleavage of TANK
- 论文作者：Li Huang ; Qinfang Liu ; Lijie Zhang ; Quan Zhang ; Liang Hu ; Changyao Li ; Shengnan Wang ; Jiangnan Li ; Yuanfeng Zhang ; Huibin Yu ; Yan Wang ; Zhaohua Zhong ; Tao Xiong ; Xueslian Xia ; Xiaojun Wang ; Li Yu ; Guohua Deng ; Xuehui Cai ; Shangjin Cui ; Changjiang Weng
- 英文论文作者：Li Huang ; Qinfang Liu ; Lijie Zhang ; Quan Zhang ; Liang Hu ; Changyao Li ; Shengnan Wang ; Jiangnan Li ; Yuanfeng Zhang ; Huibin Yu ; Yan Wang ; Zhaohua Zhong ; Tao Xiong ; Xueslian Xia ; Xiaojun Wang ; Li Yu ; Guohua Deng ; Xuehui Cai ; Shangjin Cui ; Changjiang Weng ; State Key Laboratory of Veterinary Biotechnology ; Harbin Veterinary Research Institute of Chinese Academy of Agricultural Sciences ; College of Life Sciences ; Yangtze University ; Faculty of Life Science and Technology ; Kunming University of Science and Technology ; Department of Microbiology ; Harbin Medical University
- 年：2016
- 作者机构：State Key Laboratory of Veterinary Biotechnology,Harbin Veterinary Research Institute of Chinese Academy of Agricultural Sciences;College of Life Sciences,Yangtze University;Faculty of Life Science and Technology,Kunming University of Science and Technology;Department of Microbiology,Harbin Medical University;
- 英文论文关键词：encephalomyocarditis virus ; 3C protease ; cleavage ; TANK ; TRAF6 ; NF-κB
- 会议召开时间：2016-10-19
- 会议录名称：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论文集
- 语种：英文
- 分类号：S852.65
- 学会代码：ZGXJ
- 会议名称：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
- 会议地点：中国云南昆明
- 主办单位：中国畜牧兽医学会生物技术学分会、中国免疫学会兽医免疫分会、中国农业科学院哈尔滨兽医研究所、兽医生物技术国家重点实验室
- 学会名称：中国畜牧兽医学会
- 页数：21
- 文件大小：7248k
- 原文格式：O
- 会议级别：全国
摘要
TKAF family member-associated NF-kB activator(TANK) is a negative regulator of canonical NF-kB signaling in the Toll-like receptor(TLR)-and B-cell receptor(BLR)-mediated signaling pathways.However,functions of TANK in viral infection-mediated NF-kB 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 prolease activity.In addition,EMCV 3C impaired the ability of TANK to inhibit TRAF6-mediated NF-kB 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-kB activation.
TKAF family member-associated NF-kB activator(TANK) is a negative regulator of canonical NF-kB signaling in the Toll-like receptor(TLR)-and B-cell receptor(BLR)-mediated signaling pathways.However,functions of TANK in viral infection-mediated NF-kB 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 prolease activity.In addition,EMCV 3C impaired the ability of TANK to inhibit TRAF6-mediated NF-kB 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-kB activation.
TKAF family member-associated NF-kB activator(TANK) is a negative regulator of canonical NF-kB signaling in the Toll-like receptor(TLR)-and B-cell receptor(BLR)-mediated signaling pathways.However,functions of TANK in viral infection-mediated NF-kB 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 prolease activity.In addition,EMCV 3C impaired the ability of TANK to inhibit TRAF6-mediated NF-kB 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-kB activation.
引文