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@ARTICLE{Pfannkuche:15093,
      author       = {Pfannkuche, A. and Büther, K. and Karthe, J. and Poenisch,
                      M. and Bartenschlager, R. and Trilling, M. and Hengel, H.
                      and Willbold, D. and Häussinger, D. and Bode, J. G.},
      title        = {{C}-{S}rc is required for complex formation between the
                      hepatitis {C} virus–encoded proteins {NS}5{A} and
                      {NS}5{B}: {A} prerequisite for replication},
      journal      = {Hepatology},
      volume       = {53},
      issn         = {0270-9139},
      address      = {New York [u.a.]},
      publisher    = {Wiley Interscience},
      reportid     = {PreJuSER-15093},
      pages        = {1127 - 1136},
      year         = {2011},
      note         = {Supported by the German Research Foundation through the
                      following grants: FOR 729 (Teilprojekt 7 to J. B. and D.
                      H.), SFB 575, and GK 1045 and SFB 638 (Teilprojekt 5 to R.
                      B.). M. P. is supported by the Postdoc Fellowship of the
                      Medical Faculty of Heidelberg. J. B. is supported by the
                      Heisenberg Program of the German Research Foundation.},
      abstract     = {Hepatitis C virus (HCV) is a leading cause of chronic liver
                      disease worldwide and establishes a persistent infection in
                      more than $60\%$ of infected individuals. This high
                      frequency of persistent infection indicates that HCV has
                      evolved efficient strategies to interfere with the adaptive
                      and innate immune response and to occupy and use host cell
                      infrastructure. The present study provides evidence that
                      c-Src, a member of the Src family kinases that participates
                      in many signal transduction pathways, represents an
                      essential host factor exploited for viral replication. c-Src
                      directly interacts with the viral RNA-dependent RNA
                      polymerase (NS5B) via its SH3 domain and with the
                      nonstructural phosphoprotein NS5A via its SH2 domain. Both
                      interactions are required to maintain the protein-protein
                      interaction of NS5A and NS5B, which has been previously
                      demonstrated to be essential for viral replication.
                      Accordingly, HCV genome replication and production of the
                      viral proteins was strongly reduced upon small interfering
                      RNA-mediated knockdown of c-Src or in the presence of the
                      tyrosine kinase inhibitor herbimycin A. This effect could
                      not be rescued by supplementation of the two other
                      ubiquitously expressed Src family kinases Fyn or Yes.
                      CONCLUSION: Our data suggest that c-Src participates in the
                      formation of an NS5A/NS5B protein complex that is required
                      for efficient replication of HCV.},
      keywords     = {Benzoquinones: pharmacology / Cell Line, Tumor /
                      Hepacivirus: genetics / Hepacivirus: physiology / Humans /
                      Lactams, Macrocyclic: pharmacology / RNA Replicase: genetics
                      / Viral Nonstructural Proteins / Virus Replication / src
                      Homology Domains: genetics / src-Family Kinases: physiology
                      / Benzoquinones (NLM Chemicals) / Lactams, Macrocyclic (NLM
                      Chemicals) / NS-5 protein, hepatitis C virus (NLM Chemicals)
                      / Viral Nonstructural Proteins (NLM Chemicals) / herbimycin
                      (NLM Chemicals) / src-Family Kinases (NLM Chemicals) / RNA
                      Replicase (NLM Chemicals) / J (WoSType)},
      cin          = {ICS-6},
      ddc          = {610},
      cid          = {I:(DE-Juel1)ICS-6-20110106},
      pnm          = {Funktion und Dysfunktion des Nervensystems / BioSoft:
                      Makromolekulare Systeme und biologische
                      Informationsverarbeitung},
      pid          = {G:(DE-Juel1)FUEK409 / G:(DE-Juel1)FUEK505},
      shelfmark    = {Gastroenterology $\&$ Hepatology},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:21480319},
      UT           = {WOS:000289419600008},
      doi          = {10.1002/hep.24214},
      url          = {https://juser.fz-juelich.de/record/15093},
}