Encephalomyocarditis Virus 3C Protease relieves TANK Inhibitory Effect on TRAF6-mediated NF-kappaB Signaling through Cleavage of TANK
نویسندگان
چکیده
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 http://www.jbc.org/cgi/doi/10.1074/jbc.M115.660761 The latest version is at JBC Papers in Press. Published on September 11, 2015 as Manuscript M115.660761 Copyright 2015 by The American Society for Biochemistry and Molecular Biology, Inc. by gest on A uust 7, 2017 hp://w w w .jb.org/ D ow nladed from
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Encephalomyocarditis virus 3C protease attenuates type I interferon production through disrupting the TANK–TBK1–IKKε–IRF3 complex
TRAF family member-associated NF-κB activator (TANK) is a scaffold protein that assembles into the interferon (IFN) regulator factor 3 (IRF3)-phosphorylating TANK-binding kinase 1 (TBK1)-(IκB) kinase ε (IKKε) complex, where it is involved in regulating phosphorylation of the IRF3 and IFN production. However, the functions of TANK in encephalomyocarditis virus (EMCV) infection-induced type I IFN...
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