Source:http://linkedlifedata.com/resource/pubmed/id/16375607
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
2005-12-26
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pubmed:abstractText |
Type I interferons (IFNs) induce the transcription of IFN-stimulated genes (ISGs) through activation of the Jak-Stat pathway. Although some determinants of specificity are dictated by the Jak-Stat components, recent observations indicate that the system incorporates other components for selectivity and flexibility, whose mechanisms remain to be defined. We identified a gene, beta-R1, which was induced relatively selectively by IFN-beta as compared with numerous IFN-alpha subtypes. Because all type I IFNs equally activate Jak-Stat signaling to IFN-stimulated gene factor 3 (ISGF3), this observation implied the existence of accessory signals for IFN-induced gene expression. We have used beta-R1 as a model system to examine this accessory signaling. In addition to Jak-Stat signaling for mediating IFN-induced cellular responses, p38 mitogen-activated protein kinase (p38 MAPK), phosphoinositol 3-kinase (PI3K), the IkappaB kinases (IKKs), and nuclear factor-kappaB (NF-kappaB) are some of the accessory components identified as required for the induction of certain IFN-beta-induced genes. This review focuses on the roles of accessory components in IFN-beta-mediated signaling, mechanisms of accessory signal generation, and how they modulate gene induction.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-beta,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interferon,
http://linkedlifedata.com/resource/pubmed/chemical/STAT Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/p38 Mitogen-Activated Protein...
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1079-9907
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
25
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
788-98
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:16375607-Animals,
pubmed-meshheading:16375607-Gene Expression Regulation,
pubmed-meshheading:16375607-Humans,
pubmed-meshheading:16375607-Interferon-beta,
pubmed-meshheading:16375607-MAP Kinase Signaling System,
pubmed-meshheading:16375607-Models, Biological,
pubmed-meshheading:16375607-NF-kappa B,
pubmed-meshheading:16375607-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:16375607-Protein-Tyrosine Kinases,
pubmed-meshheading:16375607-Receptors, Interferon,
pubmed-meshheading:16375607-STAT Transcription Factors,
pubmed-meshheading:16375607-Signal Transduction,
pubmed-meshheading:16375607-Transcriptional Activation,
pubmed-meshheading:16375607-p38 Mitogen-Activated Protein Kinases
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pubmed:year |
2005
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pubmed:articleTitle |
Alternative and accessory pathways in the regulation of IFN-beta-mediated gene expression.
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pubmed:affiliation |
Department of Neurosciences/NC30, Lerner Research Institute, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA.
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pubmed:publicationType |
Journal Article,
Review
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