IP6-assisted CSN-COP1 competition regulates a CRL4-ETV5 proteolytic checkpoint to safeguard glucose-induced insulin secretion

Mediators of insulin signalling are targets of cullin-RING ubiquitin ligases (CRL) that mediate protein degradation, but the role of protein degradation in insulin signalling is incompletely understood. Here, the authors identified a glucose-responsive CRL4-COP1-ETV5 proteolytic axis that promotes i...

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Autores principales:	Hong Lin, Yuan Yan, Yifan Luo, Wing Yan So, Xiayun Wei, Xiaozhe Zhang, Xiaoli Yang, Jun Zhang, Yang Su, Xiuyan Yang, Bobo Zhang, Kangjun Zhang, Nan Jiang, Billy Kwok Chong Chow, Weiping Han, Fengchao Wang, Feng Rao
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/85171494d8b0463f93a5c8fdead68f04
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spelling	oai:doaj.org-article:85171494d8b0463f93a5c8fdead68f042021-12-02T17:38:44ZIP6-assisted CSN-COP1 competition regulates a CRL4-ETV5 proteolytic checkpoint to safeguard glucose-induced insulin secretion10.1038/s41467-021-22941-32041-1723https://doaj.org/article/85171494d8b0463f93a5c8fdead68f042021-04-01T00:00:00Zhttps://doi.org/10.1038/s41467-021-22941-3https://doaj.org/toc/2041-1723Mediators of insulin signalling are targets of cullin-RING ubiquitin ligases (CRL) that mediate protein degradation, but the role of protein degradation in insulin signalling is incompletely understood. Here, the authors identified a glucose-responsive CRL4-COP1-ETV5 proteolytic axis that promotes insulin secretion, and is inhibited under hypoglycemia.Hong LinYuan YanYifan LuoWing Yan SoXiayun WeiXiaozhe ZhangXiaoli YangJun ZhangYang SuXiuyan YangBobo ZhangKangjun ZhangNan JiangBilly Kwok Chong ChowWeiping HanFengchao WangFeng RaoNature PortfolioarticleScienceQENNature Communications, Vol 12, Iss 1, Pp 1-13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Hong Lin Yuan Yan Yifan Luo Wing Yan So Xiayun Wei Xiaozhe Zhang Xiaoli Yang Jun Zhang Yang Su Xiuyan Yang Bobo Zhang Kangjun Zhang Nan Jiang Billy Kwok Chong Chow Weiping Han Fengchao Wang Feng Rao IP6-assisted CSN-COP1 competition regulates a CRL4-ETV5 proteolytic checkpoint to safeguard glucose-induced insulin secretion
description	Mediators of insulin signalling are targets of cullin-RING ubiquitin ligases (CRL) that mediate protein degradation, but the role of protein degradation in insulin signalling is incompletely understood. Here, the authors identified a glucose-responsive CRL4-COP1-ETV5 proteolytic axis that promotes insulin secretion, and is inhibited under hypoglycemia.
format	article
author	Hong Lin Yuan Yan Yifan Luo Wing Yan So Xiayun Wei Xiaozhe Zhang Xiaoli Yang Jun Zhang Yang Su Xiuyan Yang Bobo Zhang Kangjun Zhang Nan Jiang Billy Kwok Chong Chow Weiping Han Fengchao Wang Feng Rao
author_facet	Hong Lin Yuan Yan Yifan Luo Wing Yan So Xiayun Wei Xiaozhe Zhang Xiaoli Yang Jun Zhang Yang Su Xiuyan Yang Bobo Zhang Kangjun Zhang Nan Jiang Billy Kwok Chong Chow Weiping Han Fengchao Wang Feng Rao
author_sort	Hong Lin
title	IP6-assisted CSN-COP1 competition regulates a CRL4-ETV5 proteolytic checkpoint to safeguard glucose-induced insulin secretion
title_short	IP6-assisted CSN-COP1 competition regulates a CRL4-ETV5 proteolytic checkpoint to safeguard glucose-induced insulin secretion
title_full	IP6-assisted CSN-COP1 competition regulates a CRL4-ETV5 proteolytic checkpoint to safeguard glucose-induced insulin secretion
title_fullStr	IP6-assisted CSN-COP1 competition regulates a CRL4-ETV5 proteolytic checkpoint to safeguard glucose-induced insulin secretion
title_full_unstemmed	IP6-assisted CSN-COP1 competition regulates a CRL4-ETV5 proteolytic checkpoint to safeguard glucose-induced insulin secretion
title_sort	ip6-assisted csn-cop1 competition regulates a crl4-etv5 proteolytic checkpoint to safeguard glucose-induced insulin secretion
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/85171494d8b0463f93a5c8fdead68f04
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IP6-assisted CSN-COP1 competition regulates a CRL4-ETV5 proteolytic checkpoint to safeguard glucose-induced insulin secretion

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