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The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.

EPRS is a critical mTORC1–S6K1 effector that influences adiposity in mice

Arif, Abul, Terenzi, Fulvia, Potdar, Alka A., Jia, Jie, Sacks, Jessica, China, Arnab, Halawani, Dalia, Vasu, Kommireddy, Li, Xiaoxia, Brown, J. Mark, Chen, Jie, Kozma, Sara C., Thomas, George, Fox, Paul L.·2017·Nature
DOI 10.1038/nature21380PMC PMC5480610
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Crossref · 10.1038/nature21380

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  • Genetic depletion of mTORC1 subunits, deletion of S6K1 or downstream substrates, or expression of dominant negative 4E-BP1 in specific tissues extends lifespan and healthspan of mice.

    “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 [14]

    The paper reports increased lifespan in S6K1-knockout mice (Extended Data Figure 5) and in mice carrying a phosphorylation-deficient mutation in the downstream effector EPRS (main text, page unavailable). It also reports improved glucose homeostasis and reduced adiposity, but does not establish an extension of healthspan. Its EPRS mutation is not described as a tissue-specific deletion, and the paper does not report lifespan extension from dominant-negative 4E-BP1. (LLM, conf=0.86)

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  • Mice expressing EPRS S999A have reduced body weight and adipose mass, and increased lifespan, similar to mice lacking S6K1.

    “Mice expressing EPRS S999A, which is non phosphorylatable, have reduced body weight and adipose mass, and increased lifespan, similar to mice lacking S6K1 14.”

    From Targeting the biology of aging with mTOR inhibitors (2023) · cites this paper as [14]

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Research works printed but not linked: 41

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Metadata

Authors
Arif, A., Terenzi, F., Potdar, A. A., Jia, J., Sacks, J., China, A., Halawani, D., Vasu, K., Li, X., Brown, J. M., Chen, J., Kozma, S. C., Thomas, G., & Fox, P. L.
Venue
Nature
Publisher
Springer Science and Business Media LLC
Published
2017-02
Volume
542
Issue
7641
Pages
357-361
ISSN
  • 0028-0836
  • 1476-4687
DOI
10.1038/nature21380
PMC
PMC5480610
Cited by
128
References
13
Language
en
Licence
www.springer.com/tdm (tdm)

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