Regulation of lifespan in Drosophila by modulation of genes in the TOR signaling pathway.
By P. Kapahi, Brian M. Zid, Tony Harper, Daniel J. Koslover, V. Sapin, S. Benzer. Current Biology, 2004
1,381 citations recorded by the source corpus.
Subfields: Aging, Endocrine and Autonomic Systems, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/cc42e9a789d02c4fec7d2ccba658db5d75663699
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Aging
- David M. Sabatini
- Linda Partridge
- C. Kenyon
- R. Shaw
- A. Dillin
- Brian K. Kennedy
- A. Brunet
- Suzanne C Wolff
In Endocrine and Autonomic Systems
- Linda Partridge
- C. Kenyon
- David Raubenheimer
- A. Dillin
- David M. Sabatini
- Stephen J. Simpson
- A. Brunet
- Brian K. Kennedy
In Molecular Biology
- David M. Sabatini
- M. Laplante
- R. Shaw
- R. A. Saxton
- Michael N. Hall
- R. Loewith
- Steven P. Gygi
- J. Villén
Citations in the corpus
- An AMPK-FOXO pathway mediates longevity induced by a novel method of dietary restriction in C. elegans. (2007, background): “AMPK is known to regulate the TOR pathway in mammals [45], and mTOR/LET-363 and S6 kinase mutations have been found to extend lifespan in yeast, worms, and flies [44, 46–49].”
- Mechanisms of Life Span Extension by Rapamycin in the Fruit Fly Drosophila melanogaster (2010, background): “Downregulation of S6K alone is sufficient ell Metabolism 11, 35–46, January 6, 2010 ª2010 Elsevier Inc. 43 to extend life span in flies (Kapahi et al., 2004).”
- mTOR Signaling in Growth, Metabolism, and Disease. (2017, background): “Subsequent genetic studies found that reduced TOR signaling also promotes longevity in Drosophila (Kapahi et al., 2004), budding yeast, (Kaeberlin et al.”
- Lifespan extension by conditions that inhibit translation in Caenorhabditis elegans (2007, background): “The lifespan extension produced by TOR inhibition in yeast and flies has been linked to the response to DR (Kapahi et al., 2004; Kaeberlein et al., 2005).”
- Mitochondria-Ros Crosstalk in the Control of Cell Death and Aging (2011, background): “elegans, and Drosophila, TOR is required for the effects of dietary restriction, and, importantly, its downregulation extends lifespan of all these models [184] and in mice too [185].”
- Rapamycin passes the torch: a new generation of mTOR inhibitors (2011, background): “Long-term suppression of mTOR signalling (which is stimulated by nutrients) mimics dietary restriction, a well-documented means of prolonging lifespa”
- The role of mitochondria in aging. (2013, positive): “Impaired IIS and inhibition of TOR activity extend life span in worms, flies, and mammals (101, 103, 105–110).”
- Multifaceted role of mTOR (mammalian target of rapamycin) signaling pathway in human health and disease (2023, background): “169 – 171 Altogether, these studies have proved that extended life span was highly dependent on nutritional condition (glucose, fat, and protein metabolism) and a close association with the mTOR pathway.”
- Extension of chronological life span in yeast by decreased TOR pathway signaling. (2006, methodology): “elegans and Drosophila melanogaster (Vellai et al. 2003; Kapahi et al. 2004; Meissner et al. 2004), we applied a more stringent CLS protocol (see Materials and Methods) to retest the 16 strains containing deletions with putative involvement in TOR signaling.”