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  • *Caenorhabditis elegans Proteins  (1)
  • 2005-2009
  • 2000-2004  (1)
  • 1920-1924
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  • 2005-2009
  • 2000-2004  (1)
  • 1920-1924
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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2000-10-06
    Beschreibung: An insulinlike signaling pathway controls Caenorhabditis elegans aging, metabolism, and development. Mutations in the daf-2 insulin receptor-like gene or the downstream age-1 phosphoinositide 3-kinase gene extend adult life-span by two- to threefold. To identify tissues where this pathway regulates aging and metabolism, we restored daf-2 pathway signaling to only neurons, muscle, or intestine. Insulinlike signaling in neurons alone was sufficient to specify wild-type life-span, but muscle or intestinal signaling was not. However, restoring daf-2 pathway signaling to muscle rescued metabolic defects, thus decoupling regulation of life-span and metabolism. These findings point to the nervous system as a central regulator of animal longevity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolkow, C A -- Kimura, K D -- Lee, M S -- Ruvkun, G -- AG14161/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2000 Oct 6;290(5489):147-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital and Department of Genetics, Harvard Medical School, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11021802" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aging/genetics/*physiology ; Animals ; Caenorhabditis elegans/genetics/*physiology ; *Caenorhabditis elegans Proteins ; Catalase/genetics/metabolism ; Gene Expression Regulation ; Genes, Helminth ; Helminth Proteins/genetics/metabolism ; Intestines/cytology/physiology ; Larva/physiology ; Longevity ; Muscles/cytology/physiology ; Nervous System Physiological Phenomena ; Neurons/*physiology ; Phenotype ; *Phosphatidylinositol 3-Kinases ; Promoter Regions, Genetic ; Receptor, Insulin/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Superoxide Dismutase/genetics/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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