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Sci. Aging Knowl. Environ., 11 August 2004 PERSPECTIVESTicking Fast or Ticking Slow, Through Shc Must You Go?Florent M. Martin, and Jeffrey S. Friedman The authors are in the Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA. E-mail: friedman{at}scripps.edu (J.S.F.) http://sageke.sciencemag.org/cgi/content/full/2004/32/pe32Key Words: p66shc • insulin-like growth factor • p53 • mitochondria • heat shock protein
Abstract: Circumstantial evidence places the p66 isoform of the adapter protein Shc in a position to mediate the accelerated aging phenotype displayed by mice expressing shortened forms of the tumor suppressor protein p53. We present a model in which p66shc may be responsible for integrating signals from the p53 pathway with signals from the insulin-like growth factor-1/Daf pathway in mammals. A full understanding of how interactions between p53 and p66shc affect longevity will require the production of animals with mutations in the genes encoding both proteins. Citation: F. M. Martin, J. S. Friedman, Ticking Fast or Ticking Slow, Through Shc Must You Go? Sci. Aging Knowl. Environ. 2004 (32), pe32 (2004).
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Science of Aging Knowledge Environment. ISSN 1539-6150
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