hSIR2(SIRT1) functions as an NAD-dependent p53 deacetylase.

By H. Vaziri, Scott K. Dessain, E. Eaton, S. Imai, Roy A. Frye, T. Pandita, L. Guarente, R. A. Weinberg. Cell, 2001

2,660 citations recorded by the source corpus.

Subfields: Geriatrics and Gerontology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/a0dfe909832585864ce7c280462fec5b6a7ce7f6

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. Johan Auwerx
4. M. Haigis
5. E. Verdin
6. Bor Luen Tang
7. E. Seto
8. C. Cantó

In Molecular Biology

1. L. Guarente
2. W. Gu
3. Manel Esteller
4. E. Seto
5. S. Baylin
6. E. Verdin
7. D. Sinclair
8. M. Haigis

In Oncology

1. W. Gu
2. E. Seto
3. C. Brooks
4. J. Kruse
5. Yingming Zhao
6. Johan Auwerx
7. Yi Tang
8. Tony Kouzarides

Citations in the corpus

• Mammalian Sir2 homolog SIRT7 is an activator of RNA polymerase I transcription. (2006, background): “To examine whether SIRT7-mediated activation of Pol I transcription requires any enzymatic activity, we generated two mutants, SIRT7 and SIRT7, which are mutations in conserved residues that inactivate other mammalian sirtuins (Frye 1999; Vaziri et al. 2001; Liszt et al. 2005).”
• Histone-deacetylase inhibitors: novel drugs for the treatment of cancer (2002, neutral): “Histone deacetylase inhibitors induce caspase-dependent apoptosis and downregulation of DAXX in acute promyelocytic leukaemia with t(15;17).”
• SIRT1 regulates circadian clock gene expression through PER2 deacetylation. (2008, background): “The deacetylase activity of SIRT1 was required for this effect since cotransfection of SIRT1 H363Y, a catalytically inactive, dominant-negative SIRT1 mutant version ( Vaziri et al., 2001 ), virtually abolished the circadian bioluminescence oscillations generated by the Bmal1-luciferase reporter gene”
• FoxO1 protects against pancreatic beta cell failure through NeuroD and MafA induction. (2005, background): “Interestingly, this model is opposite to the mechanism by which deacetylation controls p53 function (Luo et al., 2001; Vaziri et al., 2001).”
• Acetylation is indispensable for p53 activation. (2008, background): “The acetylation levels of p53 are significantly enhanced in response to stress and correlate well with p53 activation and stabilization (Luo et al., 2000, 2001; Vaziri et al., 2001; Ito et al., 2001; Barlev et al., 2001; Knights et al., 2006; Li et al., 2007; Zhao et al., 2008; Kim et al., 2008).”
• Tumor suppressor HIC1 directly regulates SIRT1 to modulate p53-dependent DNA-damage responses. (2005, background): “In turn, the chronic increase of SIRT1, as shown in our present work and in the studies of others (Luo et al., 2001; Vaziri et al., 2001), leads to deacetylation of p53, which impedes this protein from controlling the cellular apoptotic response.”
• Glucose restriction inhibits skeletal myoblast differentiation by activating SIRT1 through AMPK-mediated regulation of Nampt. (2008, background): “…activators, 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…”