A phylogenetically conserved NAD+-dependent protein deacetylase activity in the Sir2 protein family.

By Jeffrey S. Smith, C. Brachmann, I. Ćelić, Margaret A. Kenna, S. Muhammad, V. Starai, J. Avalos, J. Escalante‐Semerena, C. Grubmeyer, C. Wolberger and 1 more. Proceedings of the National Academy of Sciences of the United States of America, 2000

776 citations recorded by the source corpus.

Subfields: Geriatrics and Gerontology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/3b4ee2be1b00b2202ae199bcef7164b32d603e4e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Geriatrics and Gerontology

1. L. Guarente
2. D. Sinclair
3. E. Verdin
4. M. Haigis
5. Johan Auwerx
6. Joseph A. Baur
7. S. Imai
8. R. Mostoslavsky

In Molecular Biology

1. L. Guarente
2. W. Gu
3. B. Spiegelman
4. E. Verdin
5. D. Sinclair
6. M. Haigis
7. Stefanie Dimmeler
8. W. Haas

Citations in the corpus

• Nutrient control of glucose homeostasis through a complex of PGC-1α and SIRT1 (2005, background): “We show here that the Sir2 homologue, SIRT1—which modulates ageing in several specie”
• Calorie restriction extends yeast life span by lowering the level of NADH. (2004, background): “It has been shown that cells lacking the NPT1 gene (encoding nicotinic acid phosphoribosyl transferase in the NAD salvage pathway) exhibit a 40% to 60% decrease in NAD levels (Smith et al. 2000; Anderson et al. 2002).”
• SIRT1 controls endothelial angiogenic functions during vascular growth. (2007, background): “, Saccharomyces cerevisiae, Caenorhabditis elegans) (Imai et al. 2000; Landry et al. 2000; Smith et al. 2000; Guarente and Picard 2005).”
• Nutrient-sensitive mitochondrial NAD+ levels dictate cell survival. (2007, background): “The founding member of the sirtuin family, Saccharomyces cerevisiae Sir2, is an NAD+-dependent histone deacetylase that mediates life span extension by mild stress and calorie re- striction (CR) (Imai et al., 2000; Lin et al., 2000; Rogina and Helfand, 2004; Smith et al., 2000; Tanny et al., 1999).”
• Hepatocyte-specific Deletion of SIRT1 Alters Fatty Acid Metabolism and Results in Hepatic Steatosis and Inflammation (2009, background): “Recent studies have demonstrated that SIRT1, a nuclear NAD+-dependent protein deacetylase (Imai et al., 2000; Landry et al., 2000; Smith et al., 2000), plays an important role in the regulation of transcriptional networks in various critical metabolic processes.”