The CREB coactivator CRTC2 links hepatic ER stress and fasting gluconeogenesis

Yiguo Wang, Liliana Vera, Wolfgang H. Fischer and Marc Montminy ()
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Yiguo Wang: Clayton Foundation Laboratories for Peptide Biology, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA
Liliana Vera: Clayton Foundation Laboratories for Peptide Biology, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA
Wolfgang H. Fischer: Clayton Foundation Laboratories for Peptide Biology, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA
Marc Montminy: Clayton Foundation Laboratories for Peptide Biology, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA

Nature, 2009, vol. 460, issue 7254, 534-537

Abstract: Fast reaction of a CREB coactivator In fasted mammals, circulating pancreatic glucagon stimulates gluconeogenesis in the liver in part through the CREB coactivator CRTC2/TORC2. CRTC2 is now shown to function as a dual sensor for fasting signals and endoplasmic reticulum (ER) stress in the liver. Crosstalk between fasting and ER stress pathways at the level of this transcriptional coactivator contributes to glucose homeostasis under lean conditions and to the development of hyperglycaemia in obesity.

Date: 2009
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DOI: 10.1038/nature08111

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