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rdf:type |
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lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0017262,
umls-concept:C0021747,
umls-concept:C0023689,
umls-concept:C0026783,
umls-concept:C0185117,
umls-concept:C0205263,
umls-concept:C0220905,
umls-concept:C0597357,
umls-concept:C1261322,
umls-concept:C1415900,
umls-concept:C1521761,
umls-concept:C2003855,
umls-concept:C2911684
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pubmed:issue |
10
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pubmed:dateCreated |
1997-3-14
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pubmed:abstractText |
Poor induction of interferon-induced 2', 5'-oligoadenylate synthetase (2-5AS) activity has been demonstrated in cells persistently infected with the mumps virus or human T-lymphotropic virus type-I (HTLV-I). The suppression of 2-5AS induction is the result of the repression of 2-5AS gene expression at the transcription level. In a general way, after the binding of interferon-alpha (IFN-alpha) to cell surface-specific receptors, expression of 2-5AS gene is thought to be regulated by some transacting factors, IFN-regulatory factors (IRF-1 and IRF-2) and the IFN-stimulated gene factor (ISGF-3, a complex consisting of STAT-1 alpha, STAT-2 and p48). To clarify the cause of the suppression mechanism(s), fluctuation in the number of IFN receptors and the levels of mRNAs in both IRF-1 and IRF-2 were examined in cells persistently infected with the mumps virus (FLMT and KBMT). There were few differences in the number of IFN receptors and the level of IRF-2 mRNA between persistently infected cells and uninfected control cells. After the treatment of cells with IFN, a slight reduction of IRF-1 mRNA was found in persistently infected cells as compared with that of the uninfected control cells.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/2',5'-Oligoadenylate Synthetase,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/IRF1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/IRF2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Regulatory Factor-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Regulatory Factor-2,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Interferon alpha-beta,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interferon,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:issn |
0385-5600
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
40
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
777-81
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:8981353-2',5'-Oligoadenylate Synthetase,
pubmed-meshheading:8981353-Cell Line,
pubmed-meshheading:8981353-DNA-Binding Proteins,
pubmed-meshheading:8981353-Enzyme Induction,
pubmed-meshheading:8981353-Humans,
pubmed-meshheading:8981353-Interferon Regulatory Factor-1,
pubmed-meshheading:8981353-Interferon Regulatory Factor-2,
pubmed-meshheading:8981353-Interferon Type I,
pubmed-meshheading:8981353-Membrane Proteins,
pubmed-meshheading:8981353-Mumps virus,
pubmed-meshheading:8981353-Phosphoproteins,
pubmed-meshheading:8981353-Polymerase Chain Reaction,
pubmed-meshheading:8981353-Receptor, Interferon alpha-beta,
pubmed-meshheading:8981353-Receptors, Interferon,
pubmed-meshheading:8981353-Recombinant Proteins,
pubmed-meshheading:8981353-Repressor Proteins,
pubmed-meshheading:8981353-Transcription, Genetic,
pubmed-meshheading:8981353-Transcription Factors,
pubmed-meshheading:8981353-Tumor Cells, Cultured
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pubmed:year |
1996
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pubmed:articleTitle |
Investigation of IFN type-I receptor and IFN regulatory factor expression relating to induction of 2', 5'-oligoadenylate synthetase in cells persistently infected with the mumps virus.
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pubmed:affiliation |
Department of Microbiology, Sapporo Medical University School of Medicine, Hokkaido, Japan.
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pubmed:publicationType |
Journal Article
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