Calorie Restriction Promotes Mammalian Cell Survival by Inducing the SIRT1 Deacetylase
By H. Cohen, Christine Miller, Kevin J. Bitterman, N. Wall, B. Hekking, B. Kessler, K. Howitz, M. Gorospe, R. de Cabo, D. Sinclair. Science, 2004
1,990 citations recorded by the source corpus.
Subfields: Aging, Geriatrics and Gerontology, Physiology
View Paper: https://www.semanticscholar.org/paper/d6397a6826a2ea7d196782327cfc5a6c81a8285a
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Citations in the corpus
- The Histone Deacetylase SIRT6 Regulates Glucose Homeostasis via Hif1α (2010, neutral): “Furthermore, this effect appears specific for SIRT6, as SIRT1-deficient MEFs do not show this phenotype.”
- Brown Remodeling of White Adipose Tissue by SirT1-Dependent Deacetylation of Pparγ (2012, positive): “SirT1 is activated by energy deficiency (Cohen et al., 2004) and deacetylates Pparg at Lys268 and Lys293.”
- Sirtuins in aging and age-related disease. (2006, background): “Ku70, a DNA repair factor, is reported to be a target for deacetylation by Sirt1, which is another mechanism by which Sirt1 might inhibit cell death (Cohen et al., 2004).”
- SIRT1 transgenic mice show phenotypes resembling calorie restriction (2007, background): “Several links between SIRT1 and metabolic processes affected by CR have been reported, and the levels of SIRT1 are induced in several tissues in CR mice or rats ( Cohen et al ., 2004 ).”
- Glucose restriction inhibits skeletal myoblast differentiation by activating SIRT1 through AMPK-mediated regulation of Nampt. (2008, background): “…the NAD+-dependent deacetylase sirtuin SIRT1 controls critical functions of mammalian cell physiology including stress resistance (Vaziri et al., 2001) (Luo et al., 2001) (Cohen et al., 2004), replicative senescence (Chua et al., 2005), aging and differentiation (Blander and Guarente, 2004).”
- Resveratrol prolongs lifespan and retards the onset of age-related markers in a short-lived vertebrate. (2006, background): “Finally, dietary restriction, the best-studied life-extension treatment, causes over-expression of SIRT1 [31], and its effects on lifespan are not additive to those of resveratrol in Drosophila [5].”
- SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function (2012, background): “This mouse further corroborates the striking parallels between resveratrol treatment, CR, and increased SIRT1 activity (Baur et al., 2006; Cohen et al., 2004; Pearson et al., 2008; Smith et al., 2009).”
- Evolutionarily conserved and nonconserved cellular localizations and functions of human SIRT proteins. (2005, background): “, 2003), has been linked to the expression of a mammalian Sir2 homologue (Cohen et al., 2004).”
- Ink4a/Arf expression is a biomarker of aging. (2004, background): “In this regard, it will also be of future interest to determine the links, if any, between Ink4a/Arf expression and known regulators of aging such as Foxo proteins and SirT1 (60, 61).”
- Tumor suppressor HIC1 directly regulates SIRT1 to modulate p53-dependent DNA-damage responses. (2005, background): “SIRT1 levels increase upon calorie restriction or nutrient starvation (Cohen et al., 2004; Nemoto et al., 2004).”
- Genomic instability and aging-like phenotype in the absence of mammalian SIRT6. (2006, positive): “…also were suggested to mediate effects of caloric restriction (CR; Sohal and Weindruch, 1996), a dietary regimen capable of extending life span in diverse organisms from yeast to mammals (Cohen et al., 2004; Howitz et al., 2003; Lin et al., 2004; Rogina and Helfand, 2004; Wood et al., 2004).”
- Sirt3 Mediates Reduction of Oxidative Damage and Prevention of Age-related Hearing Loss under Caloric Restriction (2010, background): “However, recent studies indicate that upregulation of Sirt1 in response to CR is not observed in all tissues examined (Cohen et al., 2004; Barger et al., 2008), and currently, no study has provided conclusive evidence that sirtuins play an essential role in CR-mediated aging retardation in mammals.”