SREBP1c-CRY1 signalling represses hepatic glucose production by promoting FOXO1 degradation during refeeding

The clock protein Cry regulates hepatic glucose metabolism. Here the authors show that SREBP1c, activated by insulin signalling after feeding, directly regulates Cry transcription at specific circadian time points, and that Cry represses hepatic glucose production by promoting proteasomal degradatio...

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Autores principales: Hagoon Jang, Gha Young Lee, Christopher P. Selby, Gung Lee, Yong Geun Jeon, Jae Ho Lee, Kenneth King Yip Cheng, Paul Titchenell, Morris J. Birnbaum, Aimin Xu, Aziz Sancar, Jae Bum Kim
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Publicado: Nature Portfolio 2016
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Acceso en línea:https://doaj.org/article/8d7c5bde883440f7b735e96aacbc548c
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spelling oai:doaj.org-article:8d7c5bde883440f7b735e96aacbc548c2021-12-02T14:38:35ZSREBP1c-CRY1 signalling represses hepatic glucose production by promoting FOXO1 degradation during refeeding10.1038/ncomms121802041-1723https://doaj.org/article/8d7c5bde883440f7b735e96aacbc548c2016-07-01T00:00:00Zhttps://doi.org/10.1038/ncomms12180https://doaj.org/toc/2041-1723The clock protein Cry regulates hepatic glucose metabolism. Here the authors show that SREBP1c, activated by insulin signalling after feeding, directly regulates Cry transcription at specific circadian time points, and that Cry represses hepatic glucose production by promoting proteasomal degradation of Foxo1.Hagoon JangGha Young LeeChristopher P. SelbyGung LeeYong Geun JeonJae Ho LeeKenneth King Yip ChengPaul TitchenellMorris J. BirnbaumAimin XuAziz SancarJae Bum KimNature PortfolioarticleScienceQENNature Communications, Vol 7, Iss 1, Pp 1-14 (2016)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
Hagoon Jang
Gha Young Lee
Christopher P. Selby
Gung Lee
Yong Geun Jeon
Jae Ho Lee
Kenneth King Yip Cheng
Paul Titchenell
Morris J. Birnbaum
Aimin Xu
Aziz Sancar
Jae Bum Kim
SREBP1c-CRY1 signalling represses hepatic glucose production by promoting FOXO1 degradation during refeeding
description The clock protein Cry regulates hepatic glucose metabolism. Here the authors show that SREBP1c, activated by insulin signalling after feeding, directly regulates Cry transcription at specific circadian time points, and that Cry represses hepatic glucose production by promoting proteasomal degradation of Foxo1.
format article
author Hagoon Jang
Gha Young Lee
Christopher P. Selby
Gung Lee
Yong Geun Jeon
Jae Ho Lee
Kenneth King Yip Cheng
Paul Titchenell
Morris J. Birnbaum
Aimin Xu
Aziz Sancar
Jae Bum Kim
author_facet Hagoon Jang
Gha Young Lee
Christopher P. Selby
Gung Lee
Yong Geun Jeon
Jae Ho Lee
Kenneth King Yip Cheng
Paul Titchenell
Morris J. Birnbaum
Aimin Xu
Aziz Sancar
Jae Bum Kim
author_sort Hagoon Jang
title SREBP1c-CRY1 signalling represses hepatic glucose production by promoting FOXO1 degradation during refeeding
title_short SREBP1c-CRY1 signalling represses hepatic glucose production by promoting FOXO1 degradation during refeeding
title_full SREBP1c-CRY1 signalling represses hepatic glucose production by promoting FOXO1 degradation during refeeding
title_fullStr SREBP1c-CRY1 signalling represses hepatic glucose production by promoting FOXO1 degradation during refeeding
title_full_unstemmed SREBP1c-CRY1 signalling represses hepatic glucose production by promoting FOXO1 degradation during refeeding
title_sort srebp1c-cry1 signalling represses hepatic glucose production by promoting foxo1 degradation during refeeding
publisher Nature Portfolio
publishDate 2016
url https://doaj.org/article/8d7c5bde883440f7b735e96aacbc548c
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