Regulation of interferon regulatory factor 3-dependent innate immunity by the HCV NS3/4A protease.

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Interferon regulatory factor 3 (IRF-3) is a ubiquitously expressed latent cellular transcription factor that plays a pivotal role in control of innate, type I interferon (IFN) antiviral responses. After viral infections, IRF-3 is activated by specific C-terminal phosphorylation, which induces its dimerization and nuclear translocation, whereupon IRF-3 activates the transcription of type I IFNs and a number of other antiviral effector genes. Many viruses have evolved strategies that antagonize signaling mechanisms leading to IRF-3 activation. Recent studies have shown that hepatitis C virus blocks IRF-3 activation and subsequent IFN induction by cleaving critical cellular substrates within the intracellular antiviral signaling pathways upstream of IRF-3 with its major protease, NS3/4A.

Original languageEnglish (US)
Pages (from-to)211-226
Number of pages16
JournalMethods in Molecular Biology
Volume510
StatePublished - 2009
Externally publishedYes

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Interferon Regulatory Factor-3
Innate Immunity
Peptide Hydrolases
Antiviral Agents
Interferon Type I
Dimerization
Virus Diseases
Hepacivirus
Interferons
Transcription Factors
Phosphorylation
Viruses
Genes

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Genetics

Cite this

Regulation of interferon regulatory factor 3-dependent innate immunity by the HCV NS3/4A protease. / Li, Kui.

In: Methods in Molecular Biology, Vol. 510, 2009, p. 211-226.

Research output: Contribution to journalArticle

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