ArticleCell reports2016
FOXO/DAF-16 Activation Slows Down Turnover of the Majority of Proteins in C. elegans.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
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- Transcriptional drift in aging cells: A global decontroller.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Antioxidant and Stress Resistance Properties of Flavonoids from Chinese Sea Buckthorn Leaves from the Qinghai-Tibet Plateau.Antioxidants (Basel, Switzerland) · 2024Article
- Longevity interventions modulate mechanotransduction and extracellular matrix homeostasis in C. elegans.Nature communications · 2024Article
- Transcriptional drift in aging cells: A global de-controller.bioRxiv : the preprint server for biology · 2023Article
- Article
- APPA Increases Lifespan and Stress Resistance via Lipid Metabolism and Insulin/IGF-1 Signal Pathway inInternational journal of molecular sciences · 2023Article
- Recent Progress in Regulation of Aging by Insulin/IGF-1 Signaling inMolecules and cells · 2022Review
- Intestine-specific removal of DAF-2 nearly doubles lifespan in Caenorhabditis elegans with little fitness cost.Nature communications · 2022Article
- Axenic Culture ofInternational journal of molecular sciences · 2022Article
- Mitochondrial and metabolic dysfunction in ageing and age-related diseases.Nature reviews. Endocrinology · 2022Review
- Article
- Sonneradon A Extends Lifespan ofMarine drugs · 2022Article
- Flavonol glycoside complanatoside A requires FOXO/DAF-16, NRF2/SKN-1, and HSF-1 to improve stress resistances and extend the life span ofFrontiers in pharmacology · 2022Article
- Transcriptome Analysis of Insulin Signaling-Associated Transcription Factors inInternational journal of molecular sciences · 2021Article
- Prediction of biological age by morphological staging of sarcopenia in Caenorhabditis elegans.Disease models & mechanisms · 2021Article
- Article
- Cell-to-cell variation in gene expression and the aging process.GeroScience · 2021Review
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Authors and funding
8 authors.
Funding
Abstract
Most aging hypotheses assume the accumulation of damage, resulting in gradual physiological decline and, ultimately, death. Avoiding protein damage accumulation by enhanced turnover should slow down the aging process and extend the lifespan. However, lowering translational efficiency extends rather than shortens the lifespan in C. elegans. We studied turnover of individual proteins in the long-lived daf-2 mutant by combining SILeNCe (stable isotope labeling by nitrogen in Caenorhabditiselegans) and mass spectrometry. Intriguingly, the majority of proteins displayed prolonged half-lives in daf-2, whereas others remained unchanged, signifying that longevity is not supported by high protein turnover. This slowdown was most prominent for translation-related and mitochondrial proteins. In contrast, the high turnover of lysosomal hydrolases and very low turnover of cytoskeletal proteins remained largely unchanged. The slowdown of protein dynamics and decreased abundance of the translational machinery may point to the importance of anabolic attenuation in lifespan extension, as suggested by the hyperfunction theory.
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