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Article: Zebrafish TRIF, a Golgi-localized protein, participates in IFN induction and NF-κB activation
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TitleZebrafish TRIF, a Golgi-localized protein, participates in IFN induction and NF-κB activation
 
AuthorsFan, S1
Chen, S1
Liu, Y1
Lin, Y1
Liu, H1
Guo, L1
Lin, B1
Huang, S1
Xu, A1 1
 
KeywordsMolecular Sequence Numbers
 
Issue Date2008
 
PublisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org
 
CitationJournal of Immunology, 2008, v. 180 n. 8, p. 5373-5383 [How to Cite?]
 
AbstractThe antiviral immune responses were triggered by the innate immune recognition of viral infection. The type I IFNs (IFN-β and IFN-α) are the key cytokines produced upon viral infection and consequently link innate immunity with adaptive immunity. A main antiviral system in mammals is TRIF-dependent TLRs pathway, but the TRIF-independent RIG-I pathway, has also been discovered recently. In this manuscript, our study focuses on the functional characterization of zebrafish TRIF based on the comparison of its sequence and functional evolution from zebrafish to mammals. Our experimental results show that the full length cDNA of zebrafish TRIF cloned by RACE-PCR approach encodes a protein of 556 amino acids. Luciferase reporter assay confirms that zebrafish TRIF is able to induce the IFN promoter as well as activate NF-κB response promoter. The IFN induction function of zebrafish TRIF is abolished when Ala359 is mutated to Pro or His. Laser confocal microscopy shows that zebrafish TRIF is colocalized with a Golgi apparatus marker, implying its unique subcellular localization in Golgi apparatus. In zebrafish, the mRNA expression of molecules participating in RIG-I pathway are much more sensitive and specific to polyinosine-polycytidylic acid induction compared with those in TRIF-dependent antiviral pathway. The TRIF- dependent TLR4 IFN induction signaling appears not to be functional in zebrafish, since IFN expression cannot be upregulated by LPS. These two striking findings from de novo ligand induction experiments suggest a novel antiviral mechanism in zebrafish. The Journal of Immunology, 2008, 180: 5373-5383. Copyright © 2008 by The American Association of Immunologists, Inc.
 
ISSN0022-1767
2012 Impact Factor: 5.52
2012 SCImago Journal Rankings: 3.170
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorFan, S
 
dc.contributor.authorChen, S
 
dc.contributor.authorLiu, Y
 
dc.contributor.authorLin, Y
 
dc.contributor.authorLiu, H
 
dc.contributor.authorGuo, L
 
dc.contributor.authorLin, B
 
dc.contributor.authorHuang, S
 
dc.contributor.authorXu, A
 
dc.date.accessioned2010-09-17T10:08:08Z
 
dc.date.available2010-09-17T10:08:08Z
 
dc.date.issued2008
 
dc.description.abstractThe antiviral immune responses were triggered by the innate immune recognition of viral infection. The type I IFNs (IFN-β and IFN-α) are the key cytokines produced upon viral infection and consequently link innate immunity with adaptive immunity. A main antiviral system in mammals is TRIF-dependent TLRs pathway, but the TRIF-independent RIG-I pathway, has also been discovered recently. In this manuscript, our study focuses on the functional characterization of zebrafish TRIF based on the comparison of its sequence and functional evolution from zebrafish to mammals. Our experimental results show that the full length cDNA of zebrafish TRIF cloned by RACE-PCR approach encodes a protein of 556 amino acids. Luciferase reporter assay confirms that zebrafish TRIF is able to induce the IFN promoter as well as activate NF-κB response promoter. The IFN induction function of zebrafish TRIF is abolished when Ala359 is mutated to Pro or His. Laser confocal microscopy shows that zebrafish TRIF is colocalized with a Golgi apparatus marker, implying its unique subcellular localization in Golgi apparatus. In zebrafish, the mRNA expression of molecules participating in RIG-I pathway are much more sensitive and specific to polyinosine-polycytidylic acid induction compared with those in TRIF-dependent antiviral pathway. The TRIF- dependent TLR4 IFN induction signaling appears not to be functional in zebrafish, since IFN expression cannot be upregulated by LPS. These two striking findings from de novo ligand induction experiments suggest a novel antiviral mechanism in zebrafish. The Journal of Immunology, 2008, 180: 5373-5383. Copyright © 2008 by The American Association of Immunologists, Inc.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationJournal of Immunology, 2008, v. 180 n. 8, p. 5373-5383 [How to Cite?]
 
dc.identifier.eissn1550-6606
 
dc.identifier.epage5383
 
dc.identifier.issn0022-1767
2012 Impact Factor: 5.52
2012 SCImago Journal Rankings: 3.170
 
dc.identifier.issue8
 
dc.identifier.scopuseid_2-s2.0-45949089813
 
dc.identifier.spage5373
 
dc.identifier.urihttp://hdl.handle.net/10722/90771
 
dc.identifier.volume180
 
dc.languageeng
 
dc.publisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org
 
dc.relation.ispartofJournal of Immunology
 
dc.relation.referencesReferences in Scopus
 
dc.subjectMolecular Sequence Numbers
 
dc.titleZebrafish TRIF, a Golgi-localized protein, participates in IFN induction and NF-κB activation
 
dc.typeArticle
 
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<contributor.author>Liu, Y</contributor.author>
<contributor.author>Lin, Y</contributor.author>
<contributor.author>Liu, H</contributor.author>
<contributor.author>Guo, L</contributor.author>
<contributor.author>Lin, B</contributor.author>
<contributor.author>Huang, S</contributor.author>
<contributor.author>Xu, A</contributor.author>
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Author Affiliations
  1. Sun Yat-Sen University