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Ribosomal Protein S6 Kinase 1 Signaling Regulates Mammalian Life Span
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Mimicking Caloric Restriction: The extended life span and resistance to age-related diseases in animals exposed to caloric restriction has focused attention on the biochemical mechanisms that produce these effects. Selman et al. (p. 140 ; see the Perspective by Kaeberlein and Kapahi ) explored the role of the mammalian ribosomal protein S6 kinase 1 (S6K1), which regulates protein translation and cellular energy metabolism. Female knockout mice lacking expression of S6K1 showed characteristics of animals exposed to caloric restriction, including improved health and increased longevity. The beneficial effects included reduced fat mass in spite of increased food intake. Thus, inhibition of signaling pathways activated by S6K1 might prove beneficial in protecting against age-related disease.
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“mice deficient in S6K1 (a main mTORC1 substrate) are also long-lived”
From The Hallmarks of Aging (2013) · cites this paper as Selman et al., 2009
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“Even partial inhibition of mTORC1 in genetic mouse models (e.g., S6K1−/−, mTOR+/− mLST8+/−, mTORΔ/Δ, TSC1tg) can extend lifespan and healthspan in mice 13,17–19.”
From Targeting the biology of aging with mTOR inhibitors (2023) · cites this paper as [13]
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“Studies in mice have likewise shown that genetic depletion of mTORC1 subunits, deletion of S6K1 or downstream substrates, or expression of dominant negative 4E-BP1 in specific tissues extends the lifespan and healthspan of mice 13–16.”
From Targeting the biology of aging with mTOR inhibitors (2023) · cites this paper as [13]
Experimental — accuracy not yet measuredIn the citing paper
“Depletion of ribosome subunits or interference with the target of rapamycin/ribosomal protein S6 kinase pathway, which functions to activate protein translation, were found to alter the lifespan of a variety of species including mammals (54–56).”
From Controlled DNA double-strand break induction in mice reveals post-damage transcriptome stability (2016) · cites this paper as [55]
In the citing paper
“and mice deficient in S6K1 (a main mTORC1 substrate) are also long lived.221”
From Meta-hallmarks of aging and cancer (2023) · cites this paper as [221]
In the citing paper
“However, similar evidence does not exist yet for the effects of rapamycin on mammalian aging, and other mechanisms such as inhibition of the ribosomal S6 protein kinase 1 (S6K1) implicated in protein synthesis (Selman et al., 2009), could contribute to explain the pro-longevity effects of rapamycin (see section on Deregulated Nutrient-sensing).”
From The Hallmarks of Aging (2013) · cites this paper as Selman et al., 2009
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Metadata
- Authors
- Selman, C., Tullet, J. M. A., Wieser, D., Irvine, E., Lingard, S. J., Choudhury, A. I., Claret, M., Al-Qassab, H., Carmignac, D., Ramadani, F., Woods, A., Robinson, I. C. A., Schuster, E., Batterham, R. L., Kozma, S. C., Thomas, G., Carling, D., Okkenhaug, K., Thornton, J. M., Partridge, L., Gems, D., & Withers, D. J.
- Affiliations
- University College London (GB)
- European Bioinformatics Institute (GB)
- Institute of Healthy Ageing, Centre for Diabetes and Endocrinology, Department of Medicine, University College London, London WC1E 6JJ, UK.
- Medical Research Council (GB)
- Babraham Institute (GB)
- Imperial College London (GB)
- University of Cincinnati (US)
- Corresponding author
- Selman, Colin
- Withers, Dominic J.
- ORCID
- Venue
- Science
- Published
- 2009-10-02
- Volume
- 326
- Issue
- 5949
- Pages
- 140-144
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC4954603
- OpenAlex
- W2014892893
- Cited by
- 1,120
- References
- 29
- Citations by year
- 2026: 26 · 2025: 28 · 2024: 38 · 2023: 64 · 2022: 50 · 2021: 59 · 2020: 57 · 2019: 58 · 2018: 73 · 2017: 65 · 2016: 57 · 2015: 82 · 2014: 84 · 2013: 90 · 2012: 107
- FWCI
- 29.59
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- BIROn (Birkbeck, University of London) (submittedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Kent Academic Repository (University of Kent) (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- Wellcome Trust (066750)
- Biotechnology and Biological Sciences Research Council (BBS/E/B/0000C236, BBS/E/B/0000M979)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- ribosomal protein S6 kinase 1, mTOR signaling, caloric restriction, aging, lifespan, AMPK, age-related bone loss, immune dysfunction, motor impairment, insulin resistance
- MeSH terms
- Aging, Animals, Female, Gene Expression Regulation, Insulin, Liver, Longevity, Male, Mice, Inbred C57BL, Motor Activity, Protein Kinases, Transcription, Genetic, Signal Transduction, Bone Density, Gene Expression, T-Lymphocyte Subsets, Gene Deletion, Muscle, Skeletal, Caloric Restriction, Ribosomal Protein S6 Kinases, 90-kDa, Mice, Adipose Tissue, White, AMP-Activated Protein Kinases, TOR Serine-Threonine Kinases
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