Maintenance has been completed and SciCrunch services have been restored. We apologize for any inconvenience it may have caused.

Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

The tyrosine kinase c-Src enhances RIG-I (retinoic acid-inducible gene I)-elicited antiviral signaling.

Antiviral immune responses are initiated through Toll-like receptors (TLRs) and RIG-I (retinoic acid-inducible gene-I)-like RNA helicases that recognize nucleic acids from distinct viruses. In this study, we show that the tyrosine kinase c-Src participates in antiviral responses induced by the cytoplasmic RNA helicase RIG-I. Sendai virus (SV), which is recognized by RIG-I, induced c-Src phosphorylation. Functional impairment of c-Src through chemical inhibition or transient expression of a c-Src kinase-inactive mutant attenuated production of endogenous antiviral proteins after SV infection or after expression of RIG-I or its adapter protein MAVS. Importantly, SV-stimulated synthesis of antiviral proteins was significantly impaired in cells treated with c-Src small interfering RNA and in cells from c-Src-deficient mice. In addition, we found that c-Src interacted with components of the RIG-I pathway: RIG-I, MAVS, and TRAF3 (tumor necrosis factor receptor-associated factor-3). The interaction between c-Src and TRAF3 was found to occur within the RING domain of TRAF3. Taken together, our results suggest that c-Src enhances RIG-I-mediated signaling, acting at the level of TRAF3.

Pubmed ID: 19419966

Authors

  • Johnsen IB
  • Nguyen TT
  • Bergstroem B
  • Fitzgerald KA
  • Anthonsen MW

Journal

The Journal of biological chemistry

Publication Data

July 10, 2009

Associated Grants

  • Agency: NIAID NIH HHS, Id: R01 AI067497
  • Agency: NIAID NIH HHS, Id: R01 AI067497-01
  • Agency: NIAID NIH HHS, Id: R01 AI067497-05

Mesh Terms

  • Animals
  • Antiviral Agents
  • DEAD-box RNA Helicases
  • Gene Expression Regulation
  • Genes, Reporter
  • Humans
  • Interferon Regulatory Factor-3
  • Mice
  • Models, Biological
  • RNA, Small Interfering
  • Sendai virus
  • Signal Transduction
  • TNF Receptor-Associated Factor 3
  • src-Family Kinases