ΔNp53 or p44: Priming the p53 pump

Heidi Scrable, Tsutomu Sasaki, Bernhard Maier

Research output: Contribution to journalShort survey

24 Scopus citations

Abstract

The human protein ΔNp53 and its murine counterpart p44 are isoforms of the tumor suppressor p53 lacking the transactivation domain present in the first 39 (40 in mouse) amino acids of the full-length protein. This makes them similar in structure to the ΔN isoforms of the other members of the p53 superfamily of transcription factors, p63 and p73. The principle way both the human and the murine proteins are generated is by alternative translation of the p53 mRNA utilizing a start site in exon 4. Choice of start site depends on an interaction between p53 and its cognate RNA. When the balance between ΔNp53 (p44) and full-length p53 is altered, the function of p53 as a transcription factor is disturbed. One consequence of over-expressing p44 in mice is an acceleration of the aging process and altered expression of genes in the IGF-1 signaling cascade [Maier, B., Gluba, W., Bernier, B., Turner, T., Mohammad, K., Guise, T., et al. (2004). Modulation of mammalian lifespan by the short isoform of p53. Genes & Development, 18, 306-319]. This links p53 to the single most important growth factor pathway known to regulate lifespan in lower organisms.

Original languageEnglish (US)
Pages (from-to)913-919
Number of pages7
JournalInternational Journal of Biochemistry and Cell Biology
Volume37
Issue number5 SPEC. ISS.
DOIs
StatePublished - May 2005

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Keywords

  • Aging
  • Lifespan
  • Longevity gene
  • p47
  • p53/47
  • ΔN isoform

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

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