Putting p53 in Context

  title={Putting p53 in Context},
  author={Edward R Kastenhuber and S. Lowe},
  • Edward R Kastenhuber, S. Lowe
  • Published 2017
  • Biology, Medicine
  • Cell
  • TP53 is the most frequently mutated gene in human cancer. Functionally, p53 is activated by a host of stress stimuli and, in turn, governs an exquisitely complex anti-proliferative transcriptional program that touches upon a bewildering array of biological responses. Despite the many unveiled facets of the p53 network, a clear appreciation of how and in what contexts p53 exerts its diverse effects remains unclear. How can we interpret p53's disparate activities and the consequences of its… CONTINUE READING

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    Publications referenced by this paper.
    Mutant p53: one name, many proteins.
    • 760
    • Open Access
    In Vivo Activation of the p53 Pathway by Small-Molecule Antagonists of MDM2
    • 3,530
    • Highly Influential
    • Open Access
    The p53 circuit board.
    • 82
    • Open Access
    Mdm2 promotes the rapid degradation of p53
    • 3,970
    p53 family in development
    • 55
    • Open Access
    Mutant p53 in Cancer: New Functions and Therapeutic Opportunities
    • 864
    • Open Access
    WAF1, a potential mediator of p53 tumor suppression
    • 8,093
    • Open Access
    TP53 loss creates therapeutic vulnerability in colorectal cancer
    • 131
    • Open Access
    Prevalent p53 mutants co-opt chromatin pathways to drive cancer growth
    • 181
    • Open Access
    IAPP driven metabolic reprogramming induces regression of p53 - deficient tumours in vivo
    • 94
    • Open Access