β-arrestin 2 as an activator of cGAS-STING signaling and target of viral immune evasion

Excessive interferon (IFN) responses often follow viral infection to induce pathology or even death. Here the authors show that a signaling adaptor, β-arrestin 2, enhances the cGAS/STING innate immunity signaling pathway to promote IFN-β production, but may be degraded in infected cells to serve as...

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Autores principales:	Yihua Zhang, Manman Li, Liuyan Li, Gui Qian, Yu Wang, Zijuan Chen, Jing Liu, Chao Fang, Feng Huang, Daqiao Guo, Quanming Zou, Yiwei Chu, Dapeng Yan
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2020
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/ecca9608f5234952bee68b8d7d3ab19c
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spelling	oai:doaj.org-article:ecca9608f5234952bee68b8d7d3ab19c2021-12-02T14:40:39Zβ-arrestin 2 as an activator of cGAS-STING signaling and target of viral immune evasion10.1038/s41467-020-19849-92041-1723https://doaj.org/article/ecca9608f5234952bee68b8d7d3ab19c2020-11-01T00:00:00Zhttps://doi.org/10.1038/s41467-020-19849-9https://doaj.org/toc/2041-1723Excessive interferon (IFN) responses often follow viral infection to induce pathology or even death. Here the authors show that a signaling adaptor, β-arrestin 2, enhances the cGAS/STING innate immunity signaling pathway to promote IFN-β production, but may be degraded in infected cells to serve as a target of viral immune evasion.Yihua ZhangManman LiLiuyan LiGui QianYu WangZijuan ChenJing LiuChao FangFeng HuangDaqiao GuoQuanming ZouYiwei ChuDapeng YanNature PortfolioarticleScienceQENNature Communications, Vol 11, Iss 1, Pp 1-15 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Yihua Zhang Manman Li Liuyan Li Gui Qian Yu Wang Zijuan Chen Jing Liu Chao Fang Feng Huang Daqiao Guo Quanming Zou Yiwei Chu Dapeng Yan β-arrestin 2 as an activator of cGAS-STING signaling and target of viral immune evasion
description	Excessive interferon (IFN) responses often follow viral infection to induce pathology or even death. Here the authors show that a signaling adaptor, β-arrestin 2, enhances the cGAS/STING innate immunity signaling pathway to promote IFN-β production, but may be degraded in infected cells to serve as a target of viral immune evasion.
format	article
author	Yihua Zhang Manman Li Liuyan Li Gui Qian Yu Wang Zijuan Chen Jing Liu Chao Fang Feng Huang Daqiao Guo Quanming Zou Yiwei Chu Dapeng Yan
author_facet	Yihua Zhang Manman Li Liuyan Li Gui Qian Yu Wang Zijuan Chen Jing Liu Chao Fang Feng Huang Daqiao Guo Quanming Zou Yiwei Chu Dapeng Yan
author_sort	Yihua Zhang
title	β-arrestin 2 as an activator of cGAS-STING signaling and target of viral immune evasion
title_short	β-arrestin 2 as an activator of cGAS-STING signaling and target of viral immune evasion
title_full	β-arrestin 2 as an activator of cGAS-STING signaling and target of viral immune evasion
title_fullStr	β-arrestin 2 as an activator of cGAS-STING signaling and target of viral immune evasion
title_full_unstemmed	β-arrestin 2 as an activator of cGAS-STING signaling and target of viral immune evasion
title_sort	β-arrestin 2 as an activator of cgas-sting signaling and target of viral immune evasion
publisher	Nature Portfolio
publishDate	2020
url	https://doaj.org/article/ecca9608f5234952bee68b8d7d3ab19c
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β-arrestin 2 as an activator of cGAS-STING signaling and target of viral immune evasion

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