Modulation of mammalian life span by the short isoform of p53

  1. Bernhard Maier1,
  2. Wendy Gluba1,
  3. Brian Bernier1,
  4. Terry Turner3,4,
  5. Khalid Mohammad2,
  6. Theresa Guise2,
  7. Ann Sutherland4,
  8. Michael Thorner2, and
  9. Heidi Scrable1,5
  1. Departments of 1Neuroscience, 2Medicine, 3Urology, and 4Cell Biology, University of Virginia School of Medicine, Charlottesville, Virginia 22908, USA

Abstract

Overexpression of the short isoform of p53 (p44) has unexpectedly uncovered a role for p53 in the regulation of size and life span in the mouse. Hyperactivation of the insulin-like growth factor (IGF) signaling axis by p44 sets in motion a kinase cascade that clamps potentially unimpeded growth through p21Cip1. This suggests that pathways of gene activity known to regulate longevity in lower organisms are linked in mammals via p53 to mechanisms for controlling cell proliferation. Thus, appropriate expression of the short and long p53 isoforms might maintain a balance between tumor suppression and tissue regeneration, a major requisite for long mammalian life span.

Keywords

Footnotes

  • Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.1162404.

  • ↵5 Corresponding author. E-MAIL hs2n{at}virginia.edu.; FAX (434) 982-4380.

    • Accepted December 19, 2003.
    • Received October 17, 2003.
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This Article

  1. doi: 10.1101/gad.1162404 Genes & Dev. 18: 306-319 Cold Spring Harbor Laboratory Press

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