Nicotinamide and PNC1 govern lifespan extension by calorie restriction in Saccharomyces cerevisiae

By Rozalyn M. Anderson, Kevin J. Bitterman, Jason G. Wood, Oliver Medvedik, D. Sinclair. Nature, 2003

757 citations recorded by the source corpus.

Subfields: Aging, Biological Psychiatry, Geriatrics and Gerontology

View Paper: https://www.semanticscholar.org/paper/d1f0b56cf44dd6e2de3014a241ed44cbad0d3c62

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Citations in the corpus

The secret life of NAD+: an old metabolite controlling new metabolic signaling pathways. (2010, background): “Although the mechanism is different, yeast mutant lacking the nicotinamidase Pnc1, which is essential for NAD biosynthesis from NAM in bacteria and yeast, also showed a reduced life span, most likely due to sirtuin inhibition by NAM, because artificial depletion of NAM in the Pnc1 mutant restored li”
NAD+/NADH and NADP+/NADPH in Cellular Functions and Cell Death: Regulation and Biological Consequences (2008, neutral): “Furthermore, in addition to the major effects of NAD and NADP on several factors that could play key roles in senescence, including oxidative stress, mitochondrial functions, and telomere metabolism, NAD-dependent sirtuins have emerged as a mediator of the aging process; and the genes encoding the e”
Metabolic control of muscle mitochondrial function and fatty acid oxidation through SIRT1/PGC‐1α (2007, background): “In fact, in yeast, Pnc1p, an enzyme that synthesizes NADþ from nicotinamide and ADP-ribose, is induced by caloric restric- tion, suggesting that cellular nicotinamide concentrations might modulate lifespan (Anderson et al, 2003).”
Nutrient-sensitive mitochondrial NAD+ levels dictate cell survival. (2007, background): “Increased gene dosage or enhanced activity of Sir2 extends life span in S. cerevisiae, C. elegans, and D. melanogaster (Anderson et al., 2003; Kaeberlein et al., 1999; Lin et al., 2000; Rogina and Helfand, 2004; , 1095–1107, September 21, 2007 ª2007 Elsevier Inc. 1095 Tissenbaum and Guarente, 2001;…”
Overview of caloric restriction and ageing. (2005, background): “Finally, studies of S. cervisiae by Anderson et al. (2003) detailed the afferent hormetic pathway by which CR extends the replicative life of this yeast species.”
PARPs and ADP-ribosylation: recent advances linking molecular functions to biological outcomes (2017, background): “More broadly, a number of studies have shown that modulation of cellular NAD+ levels can regulate the catalytic activities of sirtuins (Anderson et al. 2002, 2003; Araki et al. 2004; Revollo et al. 2004); presumably, similar mechanisms can regulate the catalytic activities of PARPs as well.”
SIRTUIN 1 AND SIRTUIN 3: PHYSIOLOGICAL MODULATORS OF METABOLISM (2012, background): “In yeast, the removal of nicotinamide, the rate-limiting step of the NAD salvage pathway, is catalyzed by pyrazinamidase/nicotinamidase 1 (PNC1), a nicotinamide deaminase that is upregulated in response to caloric restriction and cellular stress (13).”
Metabolic regulation of epigenetics (2012, background): “Alternatively, CR was shown to decrease nicotinamide levels and increase NAD salvage pathway flux (Anderson et al., 2003).”
Glucose restriction inhibits skeletal myoblast differentiation by activating SIRT1 through AMPK-mediated regulation of Nampt. (2008, background): “…by the observation that the nicotinamidase PNC1- the yeast functional equivalent of mammalian Nampt (also known as PBEF or visfatin)- is both necessary and sufficient for lifespan extension caused by calorie restriction and low-intensity stress in a Sir2-dependent fashion (Anderson et al., 2003).”