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NLRP11 attenuates Toll-like receptor signalling by targeting TRAF6 for degradation via the ubiquitin ligase RNF19A

Author

Listed:
  • Chenglei Wu

    (Sun Yat-sen University)

  • Zexiong Su

    (State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University)

  • Meng Lin

    (State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University)

  • Jiayu Ou

    (Sun Yat-sen University)

  • Wei Zhao

    (Sun Yat-sen University)

  • Jun Cui

    (State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University
    Sun Yat-sen University)

  • Rong-Fu Wang

    (Houston Methodist Research Institute
    Cornell University
    College of Medicine, Texas A & M University)

Abstract

The adaptor protein TRAF6 has a central function in Toll-like receptor (TLR) signalling, yet the molecular mechanisms controlling its activity and stability are unclear. Here we show that NLRP11, a primate specific gene, inhibits TLR signalling by targeting TRAF6 for degradation. NLRP11 recruits the ubiquitin ligase RNF19A to catalyze K48-linked ubiquitination of TRAF6 at multiple sites, thereby leading to the degradation of TRAF6. Furthermore, deficiency in either NLRP11 or RNF19A abrogates K48-linked ubiquitination and degradation of TRAF6, which promotes activation of NF-κB and MAPK signalling and increases the production of proinflammatory cytokines. Therefore, our findings identify NLRP11 as a conserved negative regulator of TLR signalling in primate cells and reveal a mechanism by which the NLRP11-RNF19A axis targets TRAF6 for degradation.

Suggested Citation

  • Chenglei Wu & Zexiong Su & Meng Lin & Jiayu Ou & Wei Zhao & Jun Cui & Rong-Fu Wang, 2017. "NLRP11 attenuates Toll-like receptor signalling by targeting TRAF6 for degradation via the ubiquitin ligase RNF19A," Nature Communications, Nature, vol. 8(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-02073-3
    DOI: 10.1038/s41467-017-02073-3
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