Lifespan extension by conditions that inhibit translation in Caenorhabditis elegans

By M. Hansen, S. Taubert, D. Crawford, Nataliya Libina, Seung-Jae V. Lee, C. Kenyon. Aging Cell, 2007

908 citations recorded by the source corpus.

Subfields: Aging, Endocrine and Autonomic Systems, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/ae827e0f29aa311139f8c573b4b25aaab252e81f

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. David M. Sabatini
2. R. Shaw
3. G. Lithgow
4. Rute Martins
5. W. Link
6. A. Brunet
7. Linda Partridge
8. C. Kenyon

In Endocrine and Autonomic Systems

1. David M. Sabatini
2. G. Lithgow
3. Rute Martins
4. W. Link
5. Linda Partridge
6. T. Blackwell
7. A. Brunet
8. C. Kenyon

In Molecular Biology

1. David M. Sabatini
2. R. Shaw
3. R. A. Saxton
4. Nahum Sonenberg
5. J. Villén
6. Steven P. Gygi
7. Di Chen
8. P. Kapahi

Citations in the corpus

• Mechanisms of Life Span Extension by Rapamycin in the Fruit Fly Drosophila melanogaster (2010, background): “elegans, the life span of daf-16 null mutants can be extended by reductions in TOR signaling (Hansen et al., 2007), and, similarly, rapamycin treatment can extend the life span of dFOXO null flies (C.”
• mTOR Signaling in Growth, Metabolism, and Disease (2017, background): “Indeed, CR-like regimens do not further extend lifespan in yeast, worms, or flies with reducedmTOR signaling, suggesting an overlappingmechanism (Kaeberlein et al., 2005; Hansen et al., 2007; Kapahi et al., 2004).”
• SIRT7 links H3K18 deacetylation to maintenance of oncogenic transformation (2012, positive): “Interestingly, ribosomal protein gene deletions and inhibition of translation have also been linked to lifespan extension in numerous model organisms, including mammals 25,26 , suggesting that gene repression by SIRT7 might also influence ageing-related cellular processes.”
• Multifaceted role of mTOR (mammalian target of rapamycin) signaling pathway in human health and disease (2023, background): “170,175 There are several thoughts regarding the role of mTOR signaling in aging processes in mammalian systems.”
• Target identification using drug affinity responsive target stability (DARTS) (2009, background): “3E), the Forkhead transcription factor that mediates lifespan extension by the insulin/IGF-1 pathway (19), reminiscent of its requirement for longevity in eIF4G knockdown animals (20).”
• A Low Dose of Dietary Resveratrol Partially Mimics Caloric Restriction and Retards Aging Parameters in Mice (2008, background): “elegans [40], and therefore may play a role in the resveratrol effects reported here.”
• An AMPK-FOXO pathway mediates longevity induced by a novel method of dietary restriction in C. elegans. (2007, background): “Finally, the sir-2 gene has been shown to be important to mediate certain forms of DR in a variety of species from yeast to flies [39– 42], though this observation is still subject to debate [24, 25, 43, 44].”
• LKB1 and AMPK control of mTOR signalling and growth (2009, background): “Lifespan extension has also been observed with depletion of the TORC1 downstream effectors S6K and eIF4E (Hansen et al. 2007, Pan et al. 2007, Syntichaki et al. 2007), as well as with TOR-dependent autophagy components and the Pha-4 Foxa transcription factor (Hansen et al. 2008, Sheaffer et al.…”
• TOR signaling and rapamycin influence longevity by regulating SKN-1/Nrf and DAF-16/FoxO (2012, background): “elegans, and some studies indicate that this effect requires the conserved transcription factors DAF-16/FoxO (Hansen et al., 2007; Henderson et al., 2006; Rogers et al., 2011; Tohyama et al., 2008; Wang et al., 2010) and SKN-1/Nrf (Wang et al.”
• A Role for Autophagy in the Extension of Lifespan by Dietary Restriction in C. elegans (2008, background): “Consistent with the idea that dietary restriction/TOR inhibition and direct protein synthesis activate distinct longevity pathways, the lifespan of eat-2 mutants is further extended by direct protein synthesis inhibition but not by TOR inhibition [6].”
• Pathways of cellular proteostasis in aging and disease (2018, background): “Indeed, in key lifespan extension pathways such as caloric restriction, increased proteostasis capacity is conferred, at least in part, by a general decrease in protein translation (Hansen et al., 2007; Taylor and Dillin, 2011).”
• mTOR Signaling in Growth, Metabolism, and Disease. (2017, background): “Indeed, CR-like regimens do not further extend life span in yeast, worms, or flies with reduced mTOR signaling, suggesting an overlapping mechanism (Kaeberlin et al., 2005; Hansen et al., 2007; Kapahi et al., 2004).”
• mTOR signaling in growth control and disease (2012, neutral): “elegans DRmodel (Hansen et al., 2007).”