p53 isoforms key regulators of the cell fate decision

Sebastien M. Joruiz, Jean-Christophe Bourdon (Lead / Corresponding author)

    Research output: Contribution to journalArticlepeer-review

    124 Citations (Scopus)


    It is poorly understood how a single protein, p53, can be responsive to so many stress signals and orchestrates very diverse cell responses to maintain/restore cell/tissue functions. The uncovering that TP53 gene physiologically expresses, in a tissue-dependent manner, several p53 splice variants (isoforms) provides an explanation to its pleiotropic biological activities. Here, we summarize a decade of research on p53 isoforms. The clinical studies and the diverse cellular and animal models of p53 isoforms (zebrafish, Drosophila, and mouse) lead us to realize that a p53-mediated cell response is, in fact, the sum of the intrinsic activities of the coexpressed p53 isoforms and that unbalancing expression of different p53 isoforms leads to cancer, premature aging, (neuro)degenerative diseases, inflammation, embryo malformations, or defects in tissue regeneration. Cracking the p53 isoforms' code is, thus, a necessary step to improve cancer treatment. It also opens new exciting perspectives in tissue regeneration.

    Original languageEnglish
    Article numbera026583
    Number of pages20
    JournalCold Spring Harbor Perspectives in Medicine
    Issue number8
    Early online date22 Jan 2016
    Publication statusPublished - Aug 2016


    • Cancer
    • Splicing
    • Regeneration
    • Aging
    • Neurodegeneration
    • Infectious diseases
    • Inflammation
    • EMT

    ASJC Scopus subject areas

    • General Biochemistry,Genetics and Molecular Biology


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