Abstract
Viruses that fail to block the lethal effects of the double-stranded-RNA-activated protein kinase (PKR) may be doomed; why do so many viruses go to so much trouble to downregulate this interferon-induced protein kinase? PKR may regulate cell growth and proliferation in uninfected cells, suggesting that it also participates in the antiproliferative arm of the interferon response.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Cell Transformation, Neoplastic
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Enzyme Induction
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Gene Expression Regulation, Viral*
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HSP40 Heat-Shock Proteins
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Humans
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Interferons / physiology*
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Protein Serine-Threonine Kinases / antagonists & inhibitors
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Protein Serine-Threonine Kinases / physiology*
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Repressor Proteins / physiology
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Virus Physiological Phenomena*
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eIF-2 Kinase
Substances
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DNAJC3 protein, human
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HSP40 Heat-Shock Proteins
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Repressor Proteins
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Interferons
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Protein Serine-Threonine Kinases
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eIF-2 Kinase