TRIM14 Inhibits cGAS Degradation Mediated by Selective Autophagy Receptor p62 to Promote Innate Immune Responses
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- 作者：Meixin Chen1 ; 8 ; Qingcai Meng1 ; 8 ; Yunfei Qin1 ; 6 ; 8 ; Puping Liang1 ; Peng Tan3 ; 4 ; Lian He4 ; Yubin Zhou4 ; Yongjun Chen1 ; Junjiu Huang1 ; 7 ; hjunjiu@mail.sysu.edu.cn" class="auth_mail" title="E-mail the corresponding author ; Rong-Fu Wang3 ; 4 ; 5 ; rwang3@houstonmethodist.org" class="auth_mail" title="E-mail the corresponding author ; Jun Cui1 ; 2 ; 9 ; cuij5@mail.sysu.edu.cn" class="auth_mail" title="E-mail the corresponding author
- 关键词：cGAS ; TRIM14 ; p62 ; USP14 ; type I interferon (IFN) signaling ; autophagy
- 刊名：Molecular Cell
- 出版年：2016
- 出版时间：6 October 2016
- 年：2016
- 卷：64
- 期：1
- 页码：105-119
- 全文大小：6086 K
文摘
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TRIM14 deficiency remarkably impairs cGAS-mediated type I interferon signaling
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The ubiquitination of cGAS is a signal for p62-mediated autophagic degradation
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TRIM14 recruits USP14 to cleave K48-linked ubiquitination of cGAS at K414
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TRIM14 stabilizes cGAS by disrupting cGAS-p62 interaction in the autophagosome