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论文题目: Hippo signalling governs cytosolic nucleic acid sensing through YAP/TAZ-mediated TBK1 blockade
英文论文题目: Hippo signalling governs cytosolic nucleic acid sensing through YAP/TAZ-mediated TBK1 blockade
第一作者: Zhang, Q; Meng, FS; Chen, SS; Plouffe, SW; Wu, SY; Liu, SD; Li, XR; Zhou, RY; Wang, JX; Zhao, B; Liu, JM; Qin, J; Zou, J; Feng, XH; Guan, KL; Xu, PL
英文第一作者: Zhang, Q; Meng, FS; Chen, SS; Plouffe, SW; Wu, SY; Liu, SD; Li, XR; Zhou, RY; Wang, JX; Zhao, B; Liu, JM; Qin, J; Zou, J; Feng, XH; Guan, KL; Xu, PL
联系作者: Xu, PL (reprint author), Zhejiang Univ, Inst Life Sci, Hangzhou 310058, Zhejiang, Peoples R China.
英文联系作者: Xu, PL (reprint author), Zhejiang Univ, Inst Life Sci, Hangzhou 310058, Zhejiang, Peoples R China.
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发表年度: 2017
卷: 19
期: 4
页码: 362-+
摘要: The Hippo pathway senses cellular conditions and regulates YAP/TAZ to control cellular and tissue homeostasis, while TBK1 is central for cytosolic nucleic acid sensing and antiviral defence. The correlation between cellular nutrient/physical status and host antiviral defence is interesting but not well understood. Here we find that YAP/TAZ act as natural inhibitors of TBK1 and are vital for antiviral physiology. Independent of transcriptional regulation and through the transactivation domain, YAP/TAZ associate directly with TBK1 and abolish virus-induced TBK1 activation, by preventing TBK1 Lys63-linked ubiquitylation and the binding of adaptors/substrates. Accordingly, YAP/TAZ deletion/depletion or cellular conditions inactivating YAP/TAZ through Lats1/2 kinases relieve TBK1 suppression and boost antiviral responses, whereas expression of the transcriptionally inactive YAP dampens cytosolic RNA/DNA sensing and weakens the antiviral defence in cells and zebrafish. Thus, we describe a function of YAP/TAZ and the Hippo pathway in innate immunity, by linking cellular nutrient/physical status to antiviral host defence.
英文摘要: The Hippo pathway senses cellular conditions and regulates YAP/TAZ to control cellular and tissue homeostasis, while TBK1 is central for cytosolic nucleic acid sensing and antiviral defence. The correlation between cellular nutrient/physical status and host antiviral defence is interesting but not well understood. Here we find that YAP/TAZ act as natural inhibitors of TBK1 and are vital for antiviral physiology. Independent of transcriptional regulation and through the transactivation domain, YAP/TAZ associate directly with TBK1 and abolish virus-induced TBK1 activation, by preventing TBK1 Lys63-linked ubiquitylation and the binding of adaptors/substrates. Accordingly, YAP/TAZ deletion/depletion or cellular conditions inactivating YAP/TAZ through Lats1/2 kinases relieve TBK1 suppression and boost antiviral responses, whereas expression of the transcriptionally inactive YAP dampens cytosolic RNA/DNA sensing and weakens the antiviral defence in cells and zebrafish. Thus, we describe a function of YAP/TAZ and the Hippo pathway in innate immunity, by linking cellular nutrient/physical status to antiviral host defence.
刊物名称: NATURE CELL BIOLOGY
英文刊物名称: NATURE CELL BIOLOGY
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学科: Cell Biology
英文学科: Cell Biology
影响因子: 20.06
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论文类别: Article
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