Source:http://linkedlifedata.com/resource/pubmed/id/20006836
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2009-12-16
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pubmed:abstractText |
Hepatitis C virus (HCV) is resistant to the antiviral cytokine type I interferon, representing a major clinical problem. Garaigorta and Chisari (2009) reveal that HCV uses the activation of the ds-RNA-dependent protein kinase R, which phosphorylates and inhibits the translation initiation factor eIF-2 alpha, to block translation of interferon-stimulated genes.
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pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1934-6069
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
17
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pubmed:volume |
6
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
495-7
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pubmed:meshHeading |
pubmed-meshheading:20006836-Hepacivirus,
pubmed-meshheading:20006836-Hepatitis C,
pubmed-meshheading:20006836-Humans,
pubmed-meshheading:20006836-Interferon Regulatory Factors,
pubmed-meshheading:20006836-Interferon Type I,
pubmed-meshheading:20006836-Phosphorylation,
pubmed-meshheading:20006836-eIF-2 Kinase
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pubmed:year |
2009
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pubmed:articleTitle |
Hepatitis C and evasion of the interferon system: a PKR paradigm.
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pubmed:affiliation |
Department of Molecular and Cellular Biology, Centro Nacional de Biotecnología, CSIC, Madrid, Spain.
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pubmed:publicationType |
Journal Article,
Comment
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