id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-263200-ntq1f4ix	Mao, He-Ting	HACE1 Negatively Regulates Virus-Triggered Type I IFN Signaling by Impeding the Formation of the MAVS-TRAF3 Complex	2016-05-21		.txt	text/plain	4451	320	54	To initiate an effective antiviral response, RNA viruses are recognized by pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs) and RIG-I-like receptors (RLRs), and then trigger multiple signaling pathways to promote the production of proinflammatory cytokines, including type I IFNs [1] [2] [3] [4] . In this study, we demonstrate for the first time that HACE1 contributes to negative regulation of the virus-induced type I IFN signaling via disrupting the MAVS-TRAF3 complex. HACE1 suppressed virus-induced type I IFN signaling independently of its ubiquitin E3 ligase activity. By a small-scale screening of unknown ubiquitin E3 ligases in the regulation of virus-induced type I IFN signaling by the dual-luciferase reporter, we identified HACE1 as a potential negative regulator in this pathway. By a small-scale screening of unknown ubiquitin E3 ligases in the regulation of virus-induced type I IFN signaling by the dual-luciferase reporter, we identified HACE1 as a potential negative regulator in this pathway.	./cache/cord-263200-ntq1f4ix.txt	./txt/cord-263200-ntq1f4ix.txt