Nutrient Availability Regulates SIRT1 Through a Forkhead-Dependent Pathway

By S. Nemoto, M. Fergusson, Toren Finkel. Science, 2004

702 citations recorded by the source corpus.

Subfields: Geriatrics and Gerontology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/e1397ad28c14472454e371783173d8635d51b041

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. R. Mostoslavsky
5. W. Gu
6. Toren Finkel
7. M. McBurney
8. F. Alt

In Molecular Biology

1. S. Baylin
2. Peter A. Jones
3. L. Guarente
4. W. Gu
5. E. Verdin
6. D. Sinclair
7. R. Mostoslavsky
8. A. Brunet

In Physiology

1. E. Verdin
2. D. Sinclair
3. L. Guarente
4. R. Mostoslavsky
5. Toren Finkel
6. F. Alt
7. W. Gu
8. A. Sauve

Citations in the corpus

• The Histone Deacetylase SIRT6 Regulates Glucose Homeostasis via Hif1α (2010, unknown): “Furthermore, this effect appears specific for SIRT6, as SIRT1-deficient MEFs do not show this phenotype.”
• Calorie restriction, SIRT1 and metabolism: understanding longevity (2005, background): “Two other recent reports show increases in SIRT1 protein levels in response to food deprivatio”
• 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).”
• Multiple functions of p21 in cell cycle, apoptosis and transcriptional regulation after DNA damage. (2016, background): “Then, depending on the xtent of DNA-damage, p53 arrests cell growth or induces apopotic proteins such as pP21 (G1/S arrest) and SIRT1 (a deacetylase hat inactivate p53 via a negative feed-back) [48,49].”
• A role for the NAD-dependent deacetylase Sirt1 in the regulation of autophagy (2008, background): “We have demonstrated that mice subjected to acute overnight starvation can increase their expression of Sirt1 in certain tissues (10).”
• Sirtuins: critical regulators at the crossroads between cancer and aging (2007, background): “However, in the absence of nutrients, Foxo3a translocates to the nucleus, interacts with p53, inhibits its suppressive activity and leads to increased SIRT1 expression (Nemoto et al., 2004).”
• Regulation of SIRT1 and Its Roles in Inflammation (2022, background): “In addition, P53 can form a negative feedback loop that inhibits SIRT1 transcription by binding to the P53 response element in the SIRT1 promoter (29, 30).”
• SIRTUIN 1 AND SIRTUIN 3: PHYSIOLOGICAL MODULATORS OF METABOLISM (2012, background): “In liver, SIRT1 is upregulated during negative energy balance, as occurs during fasting and calorie restriction (7, 61, 229, 233, 275).”
• Epigenetic Determinants of Cancer. (2016, background): “It complements p53 mutations (Chen et al. 2003) leading to upregulation of SIRT1 (Chen et al. 2005), which contributes to enhanced stem/progenitor cell growth (Howitz et al. 2003; Nemoto et al. 2004; Kuzmichev et al. 2005).”
• Glucose restriction inhibits skeletal myoblast differentiation by activating SIRT1 through AMPK-mediated regulation of Nampt. (2008, background): “Increased expression (Cohen et al., 2004) (Nemoto et al., 2004) coupled to increased SIRT1 activity -as we report here in GR skeletal muscle cells- may be part of a functionally coherent strategy developed by the cell to cope with reduced nutrient availability.”