Ribosomal Protein S6 Kinase 1 Signaling Regulates Mammalian Life Span

By C. Selman, Jennifer M. A. Tullet, Daniela Wieser, E. Irvine, Steven J. Lingard, A. I. Choudhury, M. Claret, Hind Al‐Qassab, D. Carmignac, Faruk Ramadani and 12 more. Science, 2009

1,128 citations recorded by the source corpus.

Subfields: Aging, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/25a601bbde024dd5f8ef9a2a615628601bcc5134

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Aging

In Molecular Biology

Citations in the corpus

AMP-activated protein kinase inhibits NF-κB signaling and inflammation: impact on healthspan and lifespan (2011, background): “[113] observed that the extension of lifespan in ribosomal protein S6 kinase 1deficient mice was most likely linked to the increased activation of AMPK since these mice displayed a strong overlap in the gene expression patterns with those induced by AICAR treatment.”
Multifaceted role of mTOR (mammalian target of rapamycin) signaling pathway in human health and disease (2023, background): “176 Also, the loss of S6K1-induced gene expression was similar to a calorie-restricted diet or pharmacological activation of AMPK.”
mTOR Signaling in Growth, Metabolism, and Disease. (2017, background): “…of evidence suggest that the general reduction in mRNA translation during mTORC1 inhibition slows aging by reducing the accumulation of proteotoxic and oxidative stress, consistent with the observation that loss of the mTORC1 substrate S6K1 also extends life span in mammals (Selman et al., 2009).”
Rapamycin, but not resveratrol or simvastatin, extends life span of genetically heterogeneous mice. (2011, background): “Because ribosomal S6 protein kinase (S6K) is among the major targets of mTOR action, a report that deletion of the gene for S6K1 increases life span in female mice (16) and retards age effects on bone, immunity, and motor function provides strong justification for additional work on mTOR pathways as”
TOR signaling and rapamycin influence longevity by regulating SKN-1/Nrf and DAF-16/FoxO (2012, background): “In model organisms ranging from yeast to mice, inhibition of TOR signaling increases life span (Bjedov et al., 2010; Harrison et al., 2009; Kapahi et al., 2010; Kenyon, 2010; Selman et al., 2009; Stanfel et al., 2009).”
The hallmarks of aging. (2013, background): “, 2012), and mice deficient in S6K1 (a main mTORC1 substrate) are also long-lived (Selman et al., 2009).”
Mechanisms of Life Span Extension by Rapamycin in the Fruit Fly Drosophila melanogaster (2010, background): “For example, upregulation of Atg8 in fly neurons extends life span and is associated with decreased amounts of insoluble ubiquinated and oxidatively damaged proteins (Simonsen et al., 2008).”
Metabolic Control of Longevity. (2016, background): “…166, August 11, 2016 The beneficial effects of rapamycin can be phenocopied in female mice by deletion of ribosomal protein S6 kinase 1 (Rps6kb1, coding for an MTOR target), a maneuver that also increases longevity (Selman et al., 2009), as well as by artificial induction of autophagy (see above).”