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Glycogen synthase kinase 3β ubiquitination by TRAF6 regulates TLR3-mediated pro-inflammatory cytokine production

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  • Ryeojin Ko

    (Ewha Womans University)

  • Jin Hee Park

    (Ewha Womans University)

  • Hyunil Ha

    (University of Pennsylvania Perelman School of Medicine)

  • Yongwon Choi

    (University of Pennsylvania Perelman School of Medicine)

  • Soo Young Lee

    (Ewha Womans University)

Abstract

TRAF6 is critical for the production of inflammatory cytokines in various TLR-mediated signalling pathways. However, it is poorly understood how TRAF6 regulates TLR3 responses. Here we demonstrate that GSK3β interacts with TRAF6 and positively regulates the TLR3-mediated signalling. Suppression of GSK3β expression or its kinase activity drastically reduces the production of inflammatory cytokines and the induction of c-Fos by decreasing ERK and p38 phosphorylation. GSK3β physically associates with TRAF6 in a TLR3 ligand poly I:C-dependent manner. TRAF6 is determined to be a direct E3 ligase for GSK3β, and TRAF6-mediated GSK3β ubiquitination is essential for poly I:C-dependent cytokine production by promoting the TLR3 adaptor protein TRIF-assembled signalling complex.

Suggested Citation

  • Ryeojin Ko & Jin Hee Park & Hyunil Ha & Yongwon Choi & Soo Young Lee, 2015. "Glycogen synthase kinase 3β ubiquitination by TRAF6 regulates TLR3-mediated pro-inflammatory cytokine production," Nature Communications, Nature, vol. 6(1), pages 1-12, November.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7765
    DOI: 10.1038/ncomms7765
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