Genetics: Influence of TOR kinase on lifespan in C. elegans
By T. Vellai, Krisztina Takács-Vellai, Yue Zhang, A. Kovács, L. Orosz, F. Müller. Nature, 2003
1,116 citations recorded by the source corpus.
Subfields: Aging, Endocrine and Autonomic Systems
View Paper: https://www.semanticscholar.org/paper/580f42057323c51b51deda5439afcc4d6abd0bf8
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
- C. Kenyon
- Linda Partridge
- Nataliya Libina
- M. Hansen
- D. Sinclair
- Brian Onken
- Monica Driscoll
In Endocrine and Autonomic Systems
- David M. Sabatini
- C. Kenyon
- Linda Partridge
- M. Hansen
- Nataliya Libina
- Brian Onken
- Monica Driscoll
- D. Sinclair
Citations in the corpus
- Lifespan extension by conditions that inhibit translation in Caenorhabditis elegans (2007, background): “These perturbations include down-regulation of insulin/IGF-1 or target of rapamycin (TOR) signaling, dietary restriction (DR), and up-regulation of stress resistance-associated pathways activated by the FOXO transcription factor DAF-16, heat-shock factor, sirtuins or c-Jun N-terminal kinase (JNK) ( ”
- Regulation of lifespan in Drosophila by modulation of genes in the TOR signaling pathway. (2004, neutral): “elegans is not suppressible by a daf-16 mutation [23].”
- mTOR Signaling in Growth, Metabolism, and Disease. (2017, background): “This was first observed through studies in the nematode C. elegans, which found that reduced expression of the homologs of mTOR (ceTOR, formerly let-363) or Raptor (daf-15) extend life span (Vellai et al., 2003; Jia et al., 2004).”
- LKB1 and AMPK control of mTOR signalling and growth (2009, background): “Conversely, suppression of TOR promotes lifespan extension in C. elegans (Vellai et al. 2003, Jia et al. 2004, Kapahi et al. 2004).”
- mTOR Signaling in Growth, Metabolism, and Disease (2017, background): “This was first observed through studies in the nematode C. elegans, which found that reduced expression of the homologs of mTOR (ceTOR, formerly let-363) or Raptor (daf-15) extend lifespan (Vellai et al., 2003; Jia et al., 2004).”
- The molecular machinery of autophagy: unanswered questions (2005, background): “Autophagy is also associated with the extension of lifespan that correlates with caloric restriction (Bergamini et al., 2003; Longo and Finch, 2003; Melendez et al., 2003; Vellai et al., 2003).”
- With TOR less is more: a key role for the conserved nutrient sensing TOR pathway in aging (2010, positive): “This effect is independent of the FOXO ortholog DAF-16 (Vellai et al., 2003), a transcription factor that is required to mediate the life span extension caused by reduced insulin-like signaling (ILS) pathway activity (Guarente and Kenyon, 2000).”