Source:http://linkedlifedata.com/resource/pubmed/id/17785777
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
|
pubmed:dateCreated |
2007-9-5
|
pubmed:abstractText |
Virus replication induces the expression of antiviral type I (IFN-alphabeta) and type III (IFN-lambda1-3 or IL-28A/B and IL-29) IFN genes via TLR-dependent and -independent pathways. Although type III IFNs differ genetically from type I IFNs, their similar biological antiviral functions suggest that their expression is regulated in a similar fashion. Structural and functional characterization of the IFN-lambda1 and IFN-lambda3 gene promoters revealed them to be similar to IFN-beta and IFN-alpha genes, respectively. Both of these promoters had functional IFN-stimulated response element and NF-kappaB binding sites. The binding of IFN regulatory factors (IRF) to type III IFN promoter IFN-stimulated response element sites was the most important event regulating the expression of these genes. Ectopic expression of the components of TLR7 (MyD88 plus IRF1/IRF7), TLR3 (Toll/IL-1R domain-containing adapter-inducing factor), or retinoic acid-inducible gene I (RIG-I) signal transduction pathways induced the activation of IFN-lambda1 promoter, whereas the IFN-lambda3 promoter was efficiently activated only by overexpression of MyD88 and IRF7. The ectopic expression of Pin1, a recently identified suppressor for IRF3-dependent antiviral response, decreased the IFN promoter activation induced by any of these three signal transduction pathways, including the MyD88-dependent one. To conclude, the data suggest that the IFN-lambda1 gene is regulated by virus-activated IRF3 and IRF7, thus resembling that of the IFN-beta gene, whereas IFN-lambda2/3 gene expression is mainly controlled by IRF7, thus resembling those of IFN-alpha genes.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
AIM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/IL28B protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/IL29 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/IRF3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/IRF7 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Regulatory Factor-3,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Regulatory Factor-7,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukins,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B
|
pubmed:status |
MEDLINE
|
pubmed:month |
Sep
|
pubmed:issn |
0022-1767
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
15
|
pubmed:volume |
179
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
3434-42
|
pubmed:dateRevised |
2008-11-21
|
pubmed:meshHeading |
pubmed-meshheading:17785777-Base Sequence,
pubmed-meshheading:17785777-Binding Sites,
pubmed-meshheading:17785777-Cell Line,
pubmed-meshheading:17785777-Cytokines,
pubmed-meshheading:17785777-Dendritic Cells,
pubmed-meshheading:17785777-Gene Expression Regulation,
pubmed-meshheading:17785777-Gene Expression Regulation, Viral,
pubmed-meshheading:17785777-Humans,
pubmed-meshheading:17785777-Interferon Regulatory Factor-3,
pubmed-meshheading:17785777-Interferon Regulatory Factor-7,
pubmed-meshheading:17785777-Interferon Type I,
pubmed-meshheading:17785777-Interleukins,
pubmed-meshheading:17785777-Molecular Sequence Data,
pubmed-meshheading:17785777-Multigene Family,
pubmed-meshheading:17785777-NF-kappa B,
pubmed-meshheading:17785777-Promoter Regions, Genetic,
pubmed-meshheading:17785777-Protein Structure, Tertiary,
pubmed-meshheading:17785777-Response Elements,
pubmed-meshheading:17785777-Sindbis Virus
|
pubmed:year |
2007
|
pubmed:articleTitle |
IFN regulatory factor family members differentially regulate the expression of type III IFN (IFN-lambda) genes.
|
pubmed:affiliation |
Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland. pamela.osterlund@ktl.fi
|
pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|