Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 285, Issue 13, Pages 9470-9476Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M109.071043
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Funding
- Chinese 973 Program [2006CB504301, 2010CB911802]
- National Natural Science Foundation of China [30630019, 30921001]
- Chinese Science and Technology Key Project [2008ZX10002-014]
- Chinese 111 project [B06018]
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Viral infection causes activation of transcription factors NF-kappa B 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-kappa B 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.
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