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Different tumor-derived p53 mutants exhibit distinct biological activities.

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Affiliations

  • 1. Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel.
      Authors
    • Halevy O 1
    (1 author)

ORCIDs linked to this article

Science, 01 Oct 1990, 250(4977):113-116
https://doi.org/10.1126/science.2218501 PMID: 2218501 

Abstract 

In its wild-type form, the protein p53 can interfere with neoplastic processes. Tumor-derived cells often express mutant p53. Full-length mutant forms of p53 isolated so far from transformed mouse cells exhibit three common properties in vitro: loss of transformation-suppressing activity, gain of pronounced transforming potential, and ability to bind the heat shock protein cognate hsc70. A tumor-derived mouse p53 variant is now described, whose site of mutation corresponds to a hot spot for p53 in human tumors. While absolutely nonsuppressing, it is only weakly transforming and exhibits no detectable hsc70 binding. The data suggest that the ability of a p53 mutant to bind endogenous p53 is not the sole determinant of its oncogenic potential. The data also support the existence of gain-of-function p53 mutants.

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Read article at publisher's site: https://doi.org/10.1126/science.2218501

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Funding 

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NCI NIH HHS (1)