Hepatitis C virus non-structural 5A abrogates signal transducer and activator of transcription-1 nuclear translocation induced by IFN-alpha through dephosphorylation.

No abstract is available for this paper.

• Publication year

  2007

• Venue

  World Journal of Gastroenterology

• Publication date

  2007-08-14

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.3748/WJG.V13.I30.4080PMID 17696225PMCID PMC4205308
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• HCV NS5A inhibits interferon-alpha signaling through suppression of STAT1 phosphorylation in hepatocyte-derived cell lines.

  2007cited by this paper
• Blocking of Interferon-Induced Jak-Stat Signaling by Japanese Encephalitis Virus NS5 through a Protein Tyrosine Phosphatase-Mediated Mechanism

  2006cited by this paper
• Inhibition of Interferon-Stimulated JAK-STAT Signaling by a Tick-Borne Flavivirus and Identification of NS5 as an Interferon Antagonist

  2005cited by this paper
• Hepatitis C virus expression suppresses interferon signaling by degrading STAT1.

  2005cited by this paper
• Analyse des mutations des domaines ISDR et V3 de la protéine NS5A du virus de l'hépatite C avant le traitement par l'interféron avec ou sans ribavirine

  2004cited by this paper
• Hepatitis C virus NS5A protein interacts with 2',5'-oligoadenylate synthetase and inhibits antiviral activity of IFN in an IFN sensitivity-determining region-independent manner.

  2004cited by this paper
• Expression of hepatitis C virus core protein inhibits interferon‐induced nuclear import of STATs

  2004cited by this paper
• Hepatitis C virus NS5A: tales of a promiscuous protein.

  2004cited by this paper
• The Ins and Outs of STAT1 Nuclear Transport

  2003cited by this paper
• [Mutation analysis of ISDR and V3 domains of hepatitis C virus NS5A region before interferon therapy with or without ribavirin].

  2003cited by this paper
• Hepatitis C virus biology

  2003cited by this paper
• Regulation of Interferon Regulatory Factor-3 by the Hepatitis C Virus Serine Protease

  2003cited by this paper
• Analysis of Sequence Configurations of the ISDR, PKR-Binding Domain, and V3 Region as Predictors of Response to Induction Interferon-α and Ribavirin Therapy in Chronic Hepatitis C Infection

  2002cited by this paper
• To Interfere and to Anti-interfere: The Interplay Between Hepatitis C Virus and Interferon

  2002cited by this paper
• Expression of HCV structural proteins impairs IFN-mediated antiviral response.

  2002cited by this paper
• Human hepatitis C virus NS5A protein alters intracellular calcium levels, induces oxidative stress, and activates STAT-3 and NF-κB

  2001cited by this paper
• Effects of Mutation in Hepatitis C Virus Nonstructural Protein 5A on Interferon Resistance Mediated by Inhibition of PKR Kinase Activity in Mammalian Cells

  2001cited by this paper
• NS5A, a nonstructural protein of hepatitis C virus, binds growth factor receptor-bound protein 2 adaptor protein in a Src homology 3 domain/ligand-dependent manner and perturbs mitogenic signaling.

  1999cited by this paper
• Inhibition of the interferon-inducible protein kinase PKR by HCV E2 protein.

  1999cited by this paper
• Evidence that hepatitis C virus resistance to interferon is mediated through repression of the PKR protein kinase by the nonstructural 5A protein.

  1997influential reference
• Molecular virology of hepatitis C virus.

  1997cited by this paper
• STAT3 Is a Serine Kinase Target in T Lymphocytes

  1997cited by this paper
• The structure, regulation and function of the Janus kinases (JAKs) and the signal transducers and activators of transcription (STATs).

  1997cited by this paper
• STAT3 serine phosphorylation by ERK-dependent and -independent pathways negatively modulates its tyrosine phosphorylation

  1997cited by this paper
• Phosphorylation of hepatitis C virus-encoded nonstructural protein NS5A

  1995cited by this paper
• Comparison of full-length sequences of interferon-sensitive and resistant hepatitis C virus 1b. Sensitivity to interferon is conferred by amino acid substitutions in the NS5A region.

  1995cited by this paper
• Maximal activation of transcription by Stat1 and Stat3 requires both tyrosine and serine phosphorylation.

  1995cited by this paper

• Molecular targeting of antiviral drugs used against hepatitis C virus infection

  2018cites this paper
• Hepatitis C virus infection

  2017influential citation
• Upregulation of the Suppressors of Cytokine Signaling 1 and 3 Is Associated with Arrest of Phosphorylated-STAT1 Nuclear Importation and Reduced Innate Response in Denguevirus-Infected Macrophages

  2016cites this paper
• The role of HCV proteins on treatment outcomes

  2015cites this paper
• Interferon sensitivity-determining region of hepatitis C virus influences virus production and interferon signaling

  2015cites this paper
• Interferon alpha (IFNα)-induced TRIM22 interrupts HCV replication by ubiquitinating NS5A

  2015cites this paper
• Response of Hepatitis C Virus to Long-Term Passage in the Presence of Alpha Interferon: Multiple Mutations and a Common Phenotype

  2013cites this paper
• γ-H2AX + CD8+ T lymphocytes cannot respond to IFN-α, IL-2 or IL-6 in chronic hepatitis C virus infection

  2013cites this paper
• Impact of host and virus genome variability on HCV replication and response to interferon.

  2013cites this paper
• Hepatitis C Virus NS5A Disrupts STAT1 Phosphorylation and Suppresses Type I Interferon Signaling

  2012cites this paper
• Investigation of Interferon-α Response by a Single Amino Acid Substitution of Nonstructural Protein 5A in Hepatitis C Virus-Infected Patients

  2011cites this paper
• Heat Shock Protein 72 Is Associated with the Hepatitis C Virus Replicase Complex and Enhances Viral RNA Replication*

  2010cites this paper
• STAT1 and pathogens, not a friendly relationship

  2010cites this paper
• Isolation and gene analysis of interferon alpha-resistant cell clones of the hepatitis C virus subgenome.

  2008cites this paper