Ribosomal protein S6 kinase 1 signaling regulates mammalian life span. Science (New York, N.Y.) [Science] Journal article

Title	Ribosomal protein S6 kinase 1 signaling regulates mammalian life span.
Author(s)	Selman C, Tullet JM, Wieser D, Irvine E, Lingard SJ, Choudhury AI, Claret M, Al-Qassab H, Carmignac D, Ramadani F, Woods A, Robinson IC, Schuster E, Batterham RL, Kozma SC, Thomas G, Carling D, Okkenhaug K, Thornton JM, Partridge L, Gems D, Withers DJ
Institution	Institute of Healthy Ageing, Centre for Diabetes and Endocrinology, Department of Medicine, University College London, London WC1E 6JJ, UK.
Source	Science 2009 Oct 2; 326(5949):140-4.
MeSH	AMP-Activated Protein Kinases Adipose Tissue, White Aging Animals Bone Density Caloric Restriction Female Gene Deletion Gene Expression Gene Expression Regulation Insulin Liver Longevity Male Mice Mice, Inbred C57BL Motor Activity Muscle, Skeletal Protein Kinases Ribosomal Protein S6 Kinases, 90-kDa Signal Transduction T-Lymphocyte Subsets Transcription, Genetic
Abstract	Caloric restriction (CR) protects against aging and disease, but the mechanisms by which this affects mammalian life span are unclear. We show in mice that deletion of ribosomal S6 protein kinase 1 (S6K1), a component of the nutrient-responsive mTOR (mammalian target of rapamycin) signaling pathway, led to increased life span and resistance to age-related pathologies, such as bone, immune, and motor dysfunction and loss of insulin sensitivity. Deletion of S6K1 induced gene expression patterns similar to those seen in CR or with pharmacological activation of adenosine monophosphate (AMP)-activated protein kinase (AMPK), a conserved regulator of the metabolic response to CR. Our results demonstrate that S6K1 influences healthy mammalian life-span and suggest that therapeutic manipulation of S6K1 and AMPK might mimic CR and could provide broad protection against diseases of aging.
Language	eng
Pub Type(s)	Journal Article Research Support, Non-U.S. Gov't
PubMed ID	19797661

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