Virus-triggered ubiquitination of TRAF3/6 by cIAP1/2 is essential for induction of interferon-beta (IFN-beta) and cellular antiviral response

J Biol Chem. 2010 Mar 26;285(13):9470-9476. doi: 10.1074/jbc.M109.071043. Epub 2010 Jan 22.

Abstract

Viral infection causes activation of transcription factors NF-kappaB and IRF3, which collaborate to induce type I interferons (IFNs) and cellular antiviral response. Here we show that knockdown of the E3 ubiquitin ligases cIAP1 and cIAP2 markedly inhibited virus-triggered activation of IRF3 and NF-kappaB as well as IFN-beta induction. Knockdown of cIAP1 and cIAP2 also inhibited cytoplasmic dsRNA-triggered cellular antiviral response. Endogenous coimmunoprecipitation experiments indicated that viral infection caused recruitment of cIAP1 and cIAP2 to TRAF3, TRAF6, and VISA. Furthermore, we demonstrated that cIAP1- and cIAP2-mediated virus-triggered ubiquitination of TRAF3 and TRAF6. These findings suggest that virus-triggered ubiquitination of TRAF3 and TRAF6 by cIAP1 and cIAP2 is essential for type I IFN induction and cellular antiviral response.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antiviral Agents / pharmacology*
  • Baculoviral IAP Repeat-Containing 3 Protein
  • Cytoplasm / metabolism
  • Cytosol / metabolism
  • Humans
  • Inhibitor of Apoptosis Proteins / metabolism*
  • Interferon-beta / metabolism*
  • NF-kappa B / metabolism*
  • RNA Interference
  • RNA, Double-Stranded / metabolism
  • Signal Transduction
  • TNF Receptor-Associated Factor 3 / metabolism*
  • TNF Receptor-Associated Factor 6 / metabolism*
  • Ubiquitin-Protein Ligases / metabolism*

Substances

  • Antiviral Agents
  • Inhibitor of Apoptosis Proteins
  • NF-kappa B
  • RNA, Double-Stranded
  • TNF Receptor-Associated Factor 3
  • TNF Receptor-Associated Factor 6
  • Interferon-beta
  • BIRC3 protein, human
  • Baculoviral IAP Repeat-Containing 3 Protein
  • Ubiquitin-Protein Ligases