PKR protein kinase is activated by hepatitis C virus and inhibits viral replication through translational control (Q24336050)

negative regulation of viral genome replication

GOA release 2020-03-11

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GOA release 2020-03-11

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Ju-Il Kang

1

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Shi-Nae Kwon

2

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Se-Hoon Park

3

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Yun Ki Kim

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Sang-Yun Choi

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Jungsuh P Kim

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Byung-Yoon Ahn

Essential role for the dsRNA-dependent protein kinase PKR in innate immunity to viral infection

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language of work or name

English

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publication date

June 2009

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published in

Virus Research

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volume

142

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page(s)

51-6

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issue

1-2

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cites work

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The pioneer translation initiation complex is functionally distinct from but structurally overlaps with the steady-state translation initiation complex

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Double-stranded-RNA-activated protein kinase PKR enhances transcriptional activation by tumor suppressor p53

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In vitro activation of the interferon-induced, double-stranded RNA-dependent protein kinase PKR by RNA from the 3' untranslated regions of human alpha-tropomyosin

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Activation of the interferon-inducible protein kinase PKR by hepatocellular carcinoma derived-hepatitis C virus core protein

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Control of PKR protein kinase by hepatitis C virus nonstructural 5A protein: molecular mechanisms of kinase regulation

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The protein kinase PKR is required for p38 MAPK activation and the innate immune response to bacterial endotoxin

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Expressional screening of interferon-stimulated genes for antiviral activity against hepatitis C virus replication

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Functional expression and RNA binding analysis of the interferon-induced, double-stranded RNA-activated, 68,000-Mr protein kinase in a cell-free system

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Deficient cytokine signaling in mouse embryo fibroblasts with a targeted deletion in the PKR gene: role of IRF-1 and NF-kappaB

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Initiation factor-independent translation mediated by the hepatitis C virus internal ribosome entry site

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Complete replication of hepatitis C virus in cell culture

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Cardif is an adaptor protein in the RIG-I antiviral pathway and is targeted by hepatitis C virus

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National Institutes of Health Consensus Development Conference Statement: Management of hepatitis C: 2002--June 10-12, 2002.

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Effects of mutation in hepatitis C virus nonstructural protein 5A on interferon resistance mediated by inhibition of PKR kinase activity in mammalian cells

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PKR-dependent mechanisms of gene expression from a subgenomic hepatitis C virus clone.

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Initiation of Protein Synthesis by Hepatitis C Virus Is Refractory to Reduced eIF2 · GTP · Met-tRNAiMet Ternary Complex Availability

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Mechanism of interferon action: autoregulation of RNA-dependent P1/eIF-2 alpha protein kinase (PKR) expression in transfected mammalian cells

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Hepatitis C virus expression and interferon antiviral action is dependent on PKR expression

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Production of infectious hepatitis C virus in tissue culture from a cloned viral genome

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Alpha interferon induces distinct translational control programs to suppress hepatitis C virus RNA replication

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Robust hepatitis C virus infection in vitro

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