The CREB coactivator TORC2 is a key regulator of fasting glucose metabolism

By Seung-Hoi Koo, Lawrence M. Flechner, Ling Qi, Xinmin Zhang, R. Screaton, Shawn Jeffries, S. Hedrick, Wu Xu, F. Boussouar, Paul K. Brindle and 2 more. Nature, 2005

1,033 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology, Surgery

View Paper: https://www.semanticscholar.org/paper/b15e4dd6747a59b0dbc2ea4c6184bc9e5c4d9e6e

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In Molecular Biology

1. D. Hardie
2. R. Shaw
3. G. Steinberg
4. S. Hawley
5. Bruce E. Kemp
6. Liangyou Rui
7. Xiang-Jiao Yang
8. J. Scott

In Physiology

1. D. Hardie
2. S. Hawley
3. G. Steinberg
4. Bruce E. Kemp
5. E. Seto
6. Judith Y. Altarejos
7. R. Shaw
8. Monica Driscoll

In Surgery

1. D. Hardie
2. R. Shaw
3. G. Steinberg
4. S. Hawley
5. Bruce E. Kemp
6. Liangyou Rui
7. B. Viollet
8. J. Scott

Citations in the corpus

• AMPK in Health and Disease. (2009, background): “Recently, CREB-regulated transcription coactivator 2 [CRTC2; formally known as transducer of regulated CREB activity 2 (TORC2)] has emerged as a critical regulator of gluconeogenesis (264).”
• Energy Metabolism in the Liver (2014, positive): “Both p300/CBP and cAMP-regulated transcriptional coactivator 2 (CRTC2) binds to CREB and stimulate the expression of PEPCK-C and G6Pase, thus increasing hepatic gluconenogenesis (121, 306).”
• Impaired regulation of hepatic glucose production in mice lacking the forkhead transcription factor Foxo1 in liver. (2007, background): “The Creb-Torc2 pathway is acutely activated by cAMP to promote HGP in a Pgc1a-dependent manner , but does not respond to insulin (Koo et al., 2005).”
• Cellular and molecular mechanisms of metformin: an overview. (2012, background): “localization and degradation of CRTC2, thereby inhibiting the gluconeogenic program [37, 38].”
• CREB and the CRTC co-activators: sensors for hormonal and metabolic signals (2011, background): “Importantly consistent with their role in modulating CREB activity, CRTCs also seem to function in the regulation of hepatic gluconeogenesi”
• AMP‐activated protein kinase – development of the energy sensor concept (2006, background): “…2003) and activation of elongation factor-2 kinase (Horman et al. 2002), and de novo glucose synthesis (gluconeogenesis) in the liver via phosphorylation of the transcriptional coactivator TORC2, which inhibits expression of genes involved in this pathway (Lochhead et al. 2000; Koo et al. 2005).”
• Metformin Induces a Dietary Restriction–Like State and the Oxidative Stress Response to Extend C. elegans Healthspan via AMPK, LKB1, and SKN-1 (2010, background): “elegans proteins orthologous to mammalian metformin targets like glycogen synthase (which is inhibited in mammals by AMPK [81,82]), TOR kinase complex TORC2 (inhibited by AMPK from promoting gluconeogenesis by inducing PEPCK and glucose-6phosphatase transcription [83]), PFK-2/FBPase-2 (a target of A”
• The mechanisms of action of metformin (2017, background): “In addition, some studies do not detect any changes in cellular ADP:ATP ratios after metformin treatment, although they can be observedwith AMPK Lipids cAMPcAMP AMP:ATP ATP ATP Glucagon AMP PKA SIK2 PKA F2,6BP F2,6BP FBP F6P G3P BPG 3PG OAA PKA PEP ADP ADP Ma-CoA Ac-CoA ADP:ATP CRTC2:CREB CRTC2:CREB”
• AMP-activated protein kinase: an energy sensor that regulates all aspects of cell function. (2011, background): “One involves phosphorylation of CRTC2 (a transcriptional coactivator of the cyclic AMP response element-binding protein CREB), causing its exclusion from the nucleus (Koo et al. 2005).”