The GCN5-CITED2-PKA signalling module controls hepatic glucose metabolism through a cAMP-induced substrate switch

GCN5 inhibits hepatic gluconeogenesis through acetylation of PGC-1α. Here the authors show that GCN5 also activates hepatic gluconeogenesis by acetylating histone H3K9, and that the affinity of GCN5 for its different substrates is regulated via phosphorylation at S275 by PKA in a CITED2-dependent ma...

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Autores principales:	Mashito Sakai, Tomoko Tujimura-Hayakawa, Takashi Yagi, Hiroyuki Yano, Masaru Mitsushima, Hiroyuki Unoki-Kubota, Yasushi Kaburagi, Hiroshi Inoue, Yoshiaki Kido, Masato Kasuga, Michihiro Matsumoto
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2016
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/8001c64b252745a788bee1e6cfee26e3
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spelling	oai:doaj.org-article:8001c64b252745a788bee1e6cfee26e32021-12-02T15:33:49ZThe GCN5-CITED2-PKA signalling module controls hepatic glucose metabolism through a cAMP-induced substrate switch10.1038/ncomms131472041-1723https://doaj.org/article/8001c64b252745a788bee1e6cfee26e32016-11-01T00:00:00Zhttps://doi.org/10.1038/ncomms13147https://doaj.org/toc/2041-1723GCN5 inhibits hepatic gluconeogenesis through acetylation of PGC-1α. Here the authors show that GCN5 also activates hepatic gluconeogenesis by acetylating histone H3K9, and that the affinity of GCN5 for its different substrates is regulated via phosphorylation at S275 by PKA in a CITED2-dependent manner.Mashito SakaiTomoko Tujimura-HayakawaTakashi YagiHiroyuki YanoMasaru MitsushimaHiroyuki Unoki-KubotaYasushi KaburagiHiroshi InoueYoshiaki KidoMasato KasugaMichihiro MatsumotoNature PortfolioarticleScienceQENNature Communications, Vol 7, Iss 1, Pp 1-15 (2016)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Mashito Sakai Tomoko Tujimura-Hayakawa Takashi Yagi Hiroyuki Yano Masaru Mitsushima Hiroyuki Unoki-Kubota Yasushi Kaburagi Hiroshi Inoue Yoshiaki Kido Masato Kasuga Michihiro Matsumoto The GCN5-CITED2-PKA signalling module controls hepatic glucose metabolism through a cAMP-induced substrate switch
description	GCN5 inhibits hepatic gluconeogenesis through acetylation of PGC-1α. Here the authors show that GCN5 also activates hepatic gluconeogenesis by acetylating histone H3K9, and that the affinity of GCN5 for its different substrates is regulated via phosphorylation at S275 by PKA in a CITED2-dependent manner.
format	article
author	Mashito Sakai Tomoko Tujimura-Hayakawa Takashi Yagi Hiroyuki Yano Masaru Mitsushima Hiroyuki Unoki-Kubota Yasushi Kaburagi Hiroshi Inoue Yoshiaki Kido Masato Kasuga Michihiro Matsumoto
author_facet	Mashito Sakai Tomoko Tujimura-Hayakawa Takashi Yagi Hiroyuki Yano Masaru Mitsushima Hiroyuki Unoki-Kubota Yasushi Kaburagi Hiroshi Inoue Yoshiaki Kido Masato Kasuga Michihiro Matsumoto
author_sort	Mashito Sakai
title	The GCN5-CITED2-PKA signalling module controls hepatic glucose metabolism through a cAMP-induced substrate switch
title_short	The GCN5-CITED2-PKA signalling module controls hepatic glucose metabolism through a cAMP-induced substrate switch
title_full	The GCN5-CITED2-PKA signalling module controls hepatic glucose metabolism through a cAMP-induced substrate switch
title_fullStr	The GCN5-CITED2-PKA signalling module controls hepatic glucose metabolism through a cAMP-induced substrate switch
title_full_unstemmed	The GCN5-CITED2-PKA signalling module controls hepatic glucose metabolism through a cAMP-induced substrate switch
title_sort	gcn5-cited2-pka signalling module controls hepatic glucose metabolism through a camp-induced substrate switch
publisher	Nature Portfolio
publishDate	2016
url	https://doaj.org/article/8001c64b252745a788bee1e6cfee26e3
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The GCN5-CITED2-PKA signalling module controls hepatic glucose metabolism through a cAMP-induced substrate switch

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