Linked Life Data

8836915

Source:http://linkedlifedata.com/resource/pubmed/id/8836915

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1997-4-3
pubmed:abstractText
The mechanism(s) by which interferon (IFN)-alpha confers resistance to viruses is currently being characterized. Previous studies have shown that binding of IFN-alpha to its high-affinity receptor activates transcription factor interferon-stimulated gene factor 3 (ISGF3), which positively regulates a number of antiviral genes including 2'-5'-oligoadenylate synthetase (2-5A synthetase). We show that mouse L cells expressing nonsecreted (intracellular) type I human IFN are less susceptible to encephalomyocarditis (EMC) virus infection and have increased levels of 2-5A synthetase. The 2-5A synthetase promoter is constitutively induced, and the antiviral effects are most likely mediated through activation of ISGF3, which occurs constitutively in cell lines expressing intracellular interferon. These data suggest that the internalization of IFN-alpha may play a role in the antiviral properties associated with IFN.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1079-9907
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
507-10
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Expression of intracellular interferon constitutively activates ISGF3 and confers resistance to EMC viral infection.
pubmed:affiliation
Department of Molecular and Medical Genetics, University of Toronto, Ontario, Canada.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't