Regulation of the Caenorhabditis elegans longevity protein DAF-16 by insulin/IGF-1 and germline signaling

By Kui Lin, H. Hsin, Nataliya Libina, C. Kenyon. Nature Genetics, 2001

1,094 citations recorded by the source corpus.

Subfields: Aging, Endocrine and Autonomic Systems, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e35c15a9a47521727d3ffe2a6068a8509e895c09

How researchers see this paper

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

In Aging

1. C. Kenyon
2. Richard I. Morimoto
3. A. Brunet
4. T. Blackwell
5. E. L. Greer
6. J. Ahringer
7. L. Guarente
8. R. Kamath

In Endocrine and Autonomic Systems

1. Richard I. Morimoto
2. C. Kenyon
3. T. Blackwell
4. G. Lithgow
5. Rute Martins
6. W. Link
7. A. Brunet
8. Coleen T. Murphy

In Molecular Biology

1. C. Kenyon
2. Richard I. Morimoto
3. W. Gu
4. L. Guarente
5. J. Ahringer
6. R. Kamath
7. T. Blackwell
8. Andrew G. Fraser

Citations in the corpus

• Mammalian SIRT1 represses forkhead transcription factors. (2004, background): “Thus, mutations in daf-2 lead to the translocation of DAF-16 to the nucleus, where it is active (Henderson and Johnson, 2001; Lin et al., 2001; Lee et al., 2001).”
• Forkhead transcription factors: key players in development and metabolism. (2002, background): “…phosphorylation sites in DAF-16 leads to its stable nuclear localization, independent of DAF-2 signaling; Lee et al. (2001) found this to correlate with a constitutive dauer phenotype in a daf-2 background, whereas Lin et al. (2001) failed to see an effect on either life span or dauer formation.”
• Direct inhibition of the longevity-promoting factor SKN-1 by insulin-like signaling in C. elegans. (2008, positive): “elegans, signaling through the IIS receptor DAF2 ultimately directs the related kinases AKT-1, -2, and SGK-1 to phosphorylate the FOXO protein DAF-16, thereby inhibiting its accumulation in nuclei (Henderson and Johnson, 2001; Hertweck et al., 2004; Lin et al., 2001; Ogg et al., 1997).”
• The plasticity of aging: insights from long-lived mutants. (2005, background): “This life span extension is largely af-16 dependent (Alcedo and Kenyon, 2004; Apfeld nd Kenyon, 1999) and is associated with DAF-16 uclear localization (Lin et al., 2001).”
• An integrated view of oxidative stress in aging: basic mechanisms, functional effects, and pathological considerations. (2007, background): “Not surprisingly, life-extension in these animals is generally accompanied by increased antioxidant defenses and resistance to oxidative stress (15, 103, 144, 258, 271).”
• Calorie restriction and aging: review of the literature and implications for studies in humans. (2003, background): “elegans, the loss of functional mutations in the insulin–IGF-I signaling pathway nearly doubled the expected life span (155).”
• FoxO transcription factors; Regulation by AKT and 14-3-3 proteins. (2011, result): “These studies were consequently confirmed also with DAF-16 and Drosophila FoxO, demonstrating the conservation of this regulatory mechanism through evolution [28–35].”
• Lifespan extension by conditions that inhibit translation in Caenorhabditis elegans (2007, background): “Moreover, DAF-16 regulates many stress-response genes (Honda & Honda, 1999; McElwee et al., 2003; Murphy et al., 2003) and DAF-16 is known to be activated by environmental stress (Henderson & Johnson, 2001; Lin et al., 2001 ).”
• Long live FOXO: unraveling the role of FOXO proteins in aging and longevity (2015, background): “…mainly as transcriptional activators by binding the consensus core recognition motif TTGTTTAC, and their activity is inhibited by the IIS pathway (Biggs et al., 1999; Brunet et al., 1999; Henderson & Johnson, 2001; Lin et al., 2001; Calnan & Brunet, 2008; Zanella et al., 2010; Webb & Brunet, 2014).”