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			PubMed Journals: J Biol Chem

  Source:		PMID: 17204473
  Download:	https://www.jbc.org/content/282/10/7576.full.pdf

    		J Biol Chem. 2007 Mar 9;282(10):7576-81.
     		Epub 2007 Jan 4.

			Viral infections activate types I and III
			interferon genes through a common mechanism.

			Onoguchi K(1), Yoneyama M, Takemura A, Akira
			S, Taniguchi T, Namiki H, Fujita T.

			Author Information
			(1) Laboratory of Molecular Genetics, Institute
			for Virus Research and Graduate School of
			Biostudies, Kyoto University, Kyoto 606-8507,
			Japan.

			Viral infections trigger innate immune responses,
			including the production of type I interferons
			(IFN-alpha and -beta) and other proinflammatory
			cytokines. Novel antiviral cytokines IFN-lambda1,
			IFN-lambda2, and IFN-lambda3 are classified
			as type III IFNs and have evolved independently
			of type I IFNs. Type III IFN genes are regulated
			at the level of transcription and induced
			by viral infection. Although the regulatory
			mechanism of type I IFNs is well elucidated,
			the expression mechanism of IFN-lambdas
			is not well understood. Here, we analyzed
			the mechanism by which IFN-lambda gene expression
			is induced by viral infections. Loss- and
			gain-of-function experiments revealed the
			involvement of RIG-I (retinoic acid-inducible
			gene I), IPS-1, TBK1, and
			interferon regulatory factor-3, key regulators
			of the virus-induced activation of type
			I IFN genes. Consistent with this, a search
			for the cis-regulatory element of the human
			ifnlambda1 revealed a cluster of interferon
			regulatory factor-binding sites and a
			NF-kappaB-binding site. Functional analysis
			demonstrated that all of these sites are
			essential for gene activation by the virus.
			These results strongly suggest that types
			I and III IFN genes are regulated by a common
			mechanism.

			DOI: 10.1074/jbc.M608618200 PMID: 17204473
			[Indexed for MEDLINE]

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