Two neurons mediate diet-restriction-induced longevity in C. elegans

By Nicholas A. Bishop, L. Guarente. Nature, 2007

684 citations recorded by the source corpus.

Subfields: Aging, Endocrine and Autonomic Systems, Physiology

View Paper: https://www.semanticscholar.org/paper/1373bc48969a082d0455d161ed295636c7a6291d

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Citations in the corpus

Direct inhibition of the longevity-promoting factor SKN-1 by insulin-like signaling in C. elegans. (2008, background): “1, PHA-4, DAF-16, and SKN-1 or their orthologs have all been shown to influence aspects of metabolism, and thereby presumably may affect the rates of damage that leads to aging (Accili and Arden, 2004; Bishop and Guarente, 2007; Kenyon, 2005; Panowski et al., 2007; van der Horst and Burgering, 2007)”
TOR signaling and rapamycin influence longevity by regulating SKN-1/Nrf and DAF-16/FoxO (2012, background): “…and IIS, in large part because daf-16 is not needed for life span to be extended by reduced TOR kinase (LET-363) activity or most DR regimens (Bishop and Guarente, 2007; Hansen et al., 2007; Honjoh et al., 2009; Kapahi et al., 2010; Kenyon, 2010; Panowski et al., 2007; Sheaffer et al., 2008;…”
SIRT1 and other sirtuins in Metabolism (2013, background): “However, some laboratories observed life span extension by nutrient limitation that was independent of SIR2 orthologs [11,20,21].”
An AMPK-FOXO pathway mediates longevity induced by a novel method of dietary restriction in C. elegans. (2007, background): “Lastly, AMPK may also regulate the other proteins recently identified as important mediators of DR, including SIR-2, PHA-4, and SKN-1.”
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): “Under oxidative stress and with reduced insulin signaling, SKN-1 accumulates in intestinal nuclei leading to SKN-1 target gene expression [35,69,71].”
Neural mechanisms of ageing and cognitive decline (2010, background): “elegans , the ASI neurons, could mediate lifespan extension in response to caloric restrictio”
Keap1/Nrf2 signaling regulates oxidative stress tolerance and lifespan in Drosophila. (2008, background): “Very recently, the Nrf2-related SKN-1 protein was found to be required for longevity induced by dietary restriction in C.elegans (Bishop and Guarente, 2007).”
The Cell Non-Autonomous Nature of Electron Transport Chain-Mediated Longevity (2011, neutral): “…in neuronal or fat tissues (Broughton et al., 2005; Hwangbo et al., 2004; Kapahi et al., 2004; Libina et al., 2003; Wolkow et al., 2000); and genetic manipulations to specific neurons which then alter the capacity for the entire animal to respond to dietary restriction (Bishop and Guarente, 2007).”
Role of Nrf2/HO-1 system in development, oxidative stress response and diseases: an evolutionarily conserved mechanism (2016, background): “They signal to peripheral tissues to increase their metabolic activity [20].”