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			PubMed Journals: J Biol Chem

  Source:		PMID: 19380580
  Download:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2713514/pdf/zbc16202.pdf

    		J Biol Chem. 2009 Jun 12;284(24):16202-9.
     		doi: 10.1074/jbc.M109.008227. Epub 2009 Apr
			20.

			Severe acute respiratory syndrome coronavirus
			M protein inhibits type I interferon production
			by impeding the formation of
			TRAF3.TANK.TBK1/IKKepsilon complex.

			Siu KL(1), Kok KH, Ng MH, Poon VK, Yuen
			KY, Zheng BJ, Jin DY.

			Author Information
			(1) Department of Biochemistry,
			The University of Hong Kong, Pokfulam,
			Hong Kong.

			Severe acute respiratory syndrome (SARS)
			coronavirus is highly pathogenic in humans
			and evades innate immunity at multiple levels.
			It has evolved various strategies to counteract
			the production and action of type I interferons,
			which mobilize the front-line defense against
			viral infection. In this study we demonstrate
			that SARS coronavirus M protein inhibits
			gene transcription of type I interferons.
			M protein potently antagonizes the activation
			of interferon-stimulated response element-dependent
			transcription by double-stranded RNA, RIG-I,
			MDA5, TBK1, IKKepsilon, and
			virus-induced signaling adaptor (VISA) but has
			no influence on the transcriptional activity of this
			element when IRF3 or IRF7 is overexpressed.
			M protein physically associates with RIG-I,
			TBK1, IKKepsilon, and TRAF3 and likely sequesters
			some of them in membrane-associated cytoplasmic
			compartments. Consequently, the expression
			of M protein prevents the formation of
			TRAF3.TANK.TBK1/IKKepsilon complex and thereby
			inhibits TBK1/IKKepsilon-dependent activation of
			IRF3/IRF7 transcription factors. Taken together,
			our findings reveal a new mechanism by which
			SARS coronavirus circumvents the production
			of type I interferons.

			DOI: 10.1074/jbc.M109.008227 PMCID: PMC2713514
			PMID: 19380580 [Indexed for MEDLINE]

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