An AMPK-FOXO pathway mediates longevity induced by a novel method of dietary restriction in C. elegans.
By E. L. Greer, Dara P. Dowlatshahi, Max R. Banko, J. Villén, Kimmi Hoang, Daniel Blanchard, Steven P. Gygi, A. Brunet. Current Biology, 2007
820 citations recorded by the source corpus.
Subfields: Aging, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/942777b0fcde3fe6e126c114fcd4e060e2f72563
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In Aging
In Molecular Biology
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- Dervis A M Salih
In Physiology
Citations in the corpus
- AMP-activated protein kinase: an energy sensor that regulates all aspects of cell function. (2011, background): “AAK-2 is also required for life span extension in response to treatment with resveratrol (an AMPK activator that is discussed further below) and to some but not all protocols of dietary restriction (Greer et al. 2007; Greer and Brunet 2009).”
- Mitochondria-Ros Crosstalk in the Control of Cell Death and Aging (2011, background): “The same kinase is able to phosphorylate FoxO factors too [200].”
- With TOR less is more: a key role for the conserved nutrient sensing TOR pathway in aging (2010, neutral): “DAF-16, the worm ortholog of FOXO, is required for the life span extension by activation of AMPK (Greer et al., 2007) and also the maximal life span extension by DR in some, but not all, DR regimes in C. elegans (Greer and Brunet, 2009).”
- How increased oxidative stress promotes longevity and metabolic health: The concept of mitochondrial hormesis (mitohormesis). (2010, background): “(Apfeld et al., 2004; Greer et al., 2007), and has been found to induce a health-promoting metabolic state particularly by inducing”
- FoxO transcription factors in the maintenance of cellular homeostasis during aging. (2008, background): “FoxO factors have been shown to be regulated by a variety of additional stress stimuli, including DNA damage, nutrient deprivation, cytokines, and hypoxia [30,33 ,34 ,35 ,36 ,37 ,38 ].”
- AMP-activated protein kinase inhibits NF-κB signaling and inflammation: impact on healthspan and lifespan (2011, background): “In Caenorhabditis elegans, the AMPK–FoxO pathway has a crucial role in the caloric restriction induced lifespan extension [74].”
- AMPK - a nutrient and energy sensor that maintains energy homeostasis (2012, neutral): “elegans and mammalian cells, AMPK upregulates genes involved in oxidative metabolism and oxidative stress resistance by regulating transcription factors of the abnormal dauer formation 16 (DAF-16)/forkhead box O (FOXO) famil”
- 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): “lifespan-extending mechanism that is DAF-16-dependent [34],”
- Long live FOXO: unraveling the role of FOXO proteins in aging and longevity (2015, background): “Germ line loss stimulates nuclear accumulation of DAF-16/FoxO and the expression of the transcription elongation/splicing factor homolog TCER-1 in intestinal cells.”
- AMPK in Health and Disease. (2009, background): “Since the constitutively active AMPK fragment 1 (1-312) is not activated by the PT1 compound, it is proposed that PT1 acts by reversing the autoinhibition of the AIS (313-335).”
- Direct inhibition of the longevity-promoting factor SKN-1 by insulin-like signaling in C. elegans. (2008, neutral): “elegans most DR protocols extend life span independently of daf-16, and therefore seemingly without input from IIS (Antebi, 2007; Bishop and Guarente, 2007; Greer et al., 2007; Houthoofd et al., 2003; Kenyon, 2005; Panowski et al., 2007).”