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

Molecular cell | Sep 16, 2005

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 RIS Download

Mesh terms: Adaptor Proteins, Signal Transducing | Amino Acid Sequence | Animals | Cell Line | DEAD Box Protein 58 | 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

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Associated grants

  • Agency: NIAID NIH HHS, Id: R01 AI062739

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