SIRT1 deacetylates and positively regulates the nuclear receptor LXR.

By Xiaoling Li, Songwen Zhang, G. Blander, J. Tse, M. Krieger, L. Guarente. Molecules and Cells, 2007

653 citations recorded by the source corpus.

Subfields: Geriatrics and Gerontology, Physiology, Surgery

View Paper: https://www.semanticscholar.org/paper/435c49be901b474014caf547dcb94910b9a81fd4

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. Johan Auwerx
2. D. Sinclair
3. C. Cantó
4. L. Guarente
5. R. Houtkooper
6. R. Mostoslavsky
7. M. McBurney
8. F. Alt

In Physiology

1. Johan Auwerx
2. D. Sinclair
3. C. Cantó
4. R. Houtkooper
5. L. Guarente
6. R. Mostoslavsky
7. F. Alt
8. Hung-Chun Chang

In Surgery

1. C. Cantó
2. Johan Auwerx
3. J. Y. Chiang

Citations in the corpus

• SIRTUIN 1 AND SIRTUIN 3: PHYSIOLOGICAL MODULATORS OF METABOLISM (2012, background): “SIRT1-null mice demonstrated abnormal cholesterol homeostasis due to the decreased expression of LXR targets and, as a consequence, a reduction of reverse cholesterol transport as well as high-density lipoproteins (194), but low-density lipoprotein cholesterol was unchanged compared with wildtype mi”
• Glucose restriction inhibits skeletal myoblast differentiation by activating SIRT1 through AMPK-mediated regulation of Nampt. (2008, background): “…neurons (Araki et al., 2004) and pancreatic β-cells (Kitamura et al., 2005), insulin secretion (Bordone et al., 2006) (Moynihan et al., 2005), lipid (Li et al., 2007) and liver metabolism (Rodgers et al., 2005), and increased physical activity during calorie restriction (Chen et al., 2005), are…”
• The NAD+-Dependent Deacetylase SIRT1 Modulates CLOCK-Mediated Chromatin Remodeling and Circadian Control (2008, background): “The remodeling of chromatin is largely elicited by enzyme-catalyzed posttranslational modifications of the core histone N-terminal tails (Kouzarides, 2007; Li et al., 2007a; Peterson and Laniel, 2004; Strahl and Allis, 2000).”
• Hepatocyte-specific Deletion of SIRT1 Alters Fatty Acid Metabolism and Results in Hepatic Steatosis and Inflammation (2009, background): “The key regulatory factors include members of the adopted orphan nuclear receptors, particularly peroxisome proliferators-activated receptor a (PPARa), farnesoid X receptor (FXR), and liver X receptor (LXR) (Chawla et al., 2001).”
• SIRT1 regulates circadian clock gene expression through PER2 deacetylation. (2008, background): “SIRT1 was found to deacetylate not only histones but also several transcriptional regulatory proteins involved in the control of metabolism, including members of the FOXO protein family (Bordone et al., 2006; Brunet et al., 2004; Motta et al., 2004), peroxisome proliferator-activated receptor gamma ”
• SIRT1 and other sirtuins in Metabolism (2013, background): “SIRT1 deacetylates LXR and activates downstream target ABCA1, an ATP-binding cassette (ABC) transporter to promote cholesterol efflux.”
• Molecular mechanisms and potential therapeutical targets in Huntington's disease. (2010, background): “One report shows that the class III HDAC SIRT1 can also be a potential modulator of the lipid metabolism and glucose homeostasis (343).”
• SIRT5 Deacetylates Carbamoyl Phosphate Synthetase 1 and Regulates the Urea Cycle (2009, neutral): “SIRT1 has numerous nuclear substrates that are important metabolic regulators, including PGC-1a, LXR, NF-kB, p53, and forkhead proteins (Brunet et al., 2004; Li et al., 2007; Luo et al., 2001; Motta et al., 2004; Rodgers et al., 2005; Vaziri et al., 2001; Yeung et al., 2004).”
• The NAD+ precursor nicotinamide riboside enhances oxidative metabolism and protects against high-fat diet induced obesity (2012, positive): “Since NR does not activate GPR109A, we speculate that NR reduces cholesterol levels through the activation of SIRT1 in liver, which influences the activity of a number of transcription factors and cofactors linked to cholesterol homeostasis (Kemper et al., 2009; Li et al., 2007; Shin et al., 2003; W”