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VISA is an adapter protein required for virus-triggered IFN-beta signaling.

Viral infection or stimulation of TLR3 triggers signaling cascades, leading to activation of the transcription factors IRF-3 and NF-kappaB, which collaborate to induce transcription of type I interferon (IFN) genes. In this study, we identified a protein termed VISA (for virus-induced signaling adaptor) as a critical component in the IFN-beta signaling pathways. VISA recruits IRF-3 to the cytoplasmic viral dsRNA sensor RIG-I. Depletion of VISA inhibits virus-triggered and RIG-I-mediated activation of IRF-3, NF-kappaB, and the IFN-beta promoter, suggesting that VISA plays a central role in virus-triggered TLR3-independent IFN-beta signaling. Our data also indicate that VISA interacts with TRIF and TRAF6 and mediates bifurcation of the TLR3-triggered NF-kappaB and IRF-3 activation pathways. These findings suggest that VISA is critically involved in both virus-triggered TLR3-independent and TLR3-mediated antiviral IFN signaling.

Pubmed ID: 16153868


  • Xu LG
  • Wang YY
  • Han KJ
  • Li LY
  • Zhai Z
  • Shu HB


Molecular cell

Publication Data

September 16, 2005

Associated Grants

  • Agency: NIAID NIH HHS, Id: R01 AI062739

Mesh Terms

  • Adaptor Proteins, Signal Transducing
  • Amino Acid Sequence
  • Animals
  • Cell Line
  • DEAD-box RNA Helicases
  • Humans
  • Interferon-beta
  • Molecular Sequence Data
  • NF-kappa B
  • Promoter Regions, Genetic
  • RNA Helicases
  • Rats
  • Sequence Alignment
  • Signal Transduction
  • TNF Receptor-Associated Factor 2
  • TNF Receptor-Associated Factor 6
  • Tissue Distribution
  • Toll-Like Receptor 3
  • Tumor Necrosis Factor-alpha
  • Viruses