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TRIM14 Inhibits cGAS Degradation Mediated by Selective Autophagy Receptor p62 to Promote Innate Immune Responses.

Author information

Affiliations

  • 1. Key Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, PRC.
      Authors
    • Chen M 1
    • Meng Q 1
    • Liang P 1
    • Chen Y 1
    (4 authors)
  • 2. Key Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, PRC; School of Life Sciences, Zhengzhou University, Zhengzhou 450001, Henan, PRC.
      Authors
    • Qin Y 2
    (1 author)
  • 3. Center for Inflammation and Epigenetics, Houston Methodist Research Institute, Houston, TX 77030, USA; Institute of Biosciences and Technology, Texas A&M University, Health Science Center, Houston, TX 77030, USA.
      Authors
    • Tan P 3
    (1 author)
  • 4. Institute of Biosciences and Technology, Texas A&M University, Health Science Center, Houston, TX 77030, USA.
      Authors
    • He L 4
    • Zhou Y 4
    (2 authors)
  • 5. Key Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, PRC; State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou 510275, PRC.
      Authors
    • Huang J 5
    (1 author)
    • Show all (7)

ORCIDs linked to this article

Molecular Cell, 22 Sep 2016, 64(1):105-119
https://doi.org/10.1016/j.molcel.2016.08.025 PMID: 27666593 

Abstract 

Cyclic GMP-AMP synthase (cGAS) is an essential DNA virus sensor that triggers type I interferon (IFN) signaling by producing cGAMP to initiate antiviral immunity. However, post-translational regulation of cGAS remains largely unknown. We report that K48-linked ubiquitination of cGAS is a recognition signal for p62-depdendent selective autophagic degradation. The induction of TRIM14 by type I IFN accelerates cGAS stabilization by recruiting USP14 to cleave the ubiquitin chains of cGAS at lysine (K) 414. Knockout of TRIM14 impairs herpes simplex virus type 1 (HSV-1)-triggered antiviral responses in a cGAS-dependent manner. Due to impaired type I IFN production, Trim14-/- mice are highly susceptible to lethal HSV-1 infection. Taken together, our findings reveal a positive feedback loop of cGAS signaling generated by TRIM14-USP14 and provide insights into the crosstalk between autophagy and type I IFN signaling in innate immunity.

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Read article at publisher's site: https://doi.org/10.1016/j.molcel.2016.08.025

Read article for free, from open access legal sources, via Unpaywall: http://www.cell.com/article/S1097276516304671/pdfUnpaywall

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