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Journal ArticleDOI

p53 mutations in cancer

Patricia A.J. Muller, +1 more
- 01 Jan 2013 - 
- Vol. 15, Iss: 1, pp 2-8
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TLDR
Some of the emerging molecular mechanisms through which mutant p53 proteins can exert oncogenic functions, including invasion, metastasis, proliferation and cell survival, are highlighted.
Abstract
In the past fifteen years, it has become apparent that tumour-associated p53 mutations can provoke activities that are different to those resulting from simply loss of wild-type tumour-suppressing p53 function. Many of these mutant p53 proteins acquire oncogenic properties that enable them to promote invasion, metastasis, proliferation and cell survival. Here we highlight some of the emerging molecular mechanisms through which mutant p53 proteins can exert these oncogenic functions.

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Citations
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References
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Journal ArticleDOI

Mdm2 promotes the rapid degradation of p53

TL;DR: It is proposed that the Mdm2-promoted degradation of p53 provides a new mechanism to ensure effective termination of the p53 signal.
Journal ArticleDOI

Regulation of p53 stability by Mdm2

TL;DR: It is shown that interaction with Mdm2 can also result in a large reduction in p53 protein levels through enhanced proteasome-dependent degradation, which may contribute to the maintenance of low p53 concentrations in normal cells.
Journal ArticleDOI

Blinded by the Light: The Growing Complexity of p53

TL;DR: Control of p53's transcriptional activity is crucial for determining which p53 response is activated, a decision that must be understood if the next generation of drugs that selectively activate or inhibit p53 are to be exploited efficiently.
Journal ArticleDOI

Crystal structure of a p53 tumor suppressor-DNA complex: Understanding tumorigenic mutations

TL;DR: The crystal structure of a complex containing the core domain of human p53 and a DNA binding site provides a framework for understanding how mutations inactivate it, and supports the hypothesis that DNA binding is critical for the biological activity of p53.
Journal ArticleDOI

Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas

TL;DR: It is indicated that p53 loss can be required for the maintenance of aggressive carcinomas, and illustrates how the cellular senescence program can act together with the innate immune system to potently limit tumour growth.
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