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Int. J. Mol. Sci. 2017, 18(12), 2759;

Control of Nucleotide Metabolism Enables Mutant p53’s Oncogenic Gain-of-Function Activity

Department of Pathology, Stony Brook University, Stony Brook, NY 11794, USA
Current address: Enzo Life Sciences, Farmingdale, NY 11735, USA.
Author to whom correspondence should be addressed.
Received: 31 October 2017 / Revised: 6 December 2017 / Accepted: 8 December 2017 / Published: 19 December 2017
(This article belongs to the Special Issue Emerging Non-Canonical Functions and Regulation of p53)
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Since its discovery as an oncoprotein in 1979, investigation into p53’s many identities has completed a full circle and today it is inarguably the most extensively studied tumor suppressor (wild-type p53 form or WTp53) and oncogene (mutant p53 form or mtp53) in cancer research. After the p53 protein was declared “Molecule of the Year” by Science in 1993, the p53 field exploded and a plethora of excellent reviews is now available on every aspect of p53 genetics and functional repertoire in a cell. Nevertheless, new functions of p53 continue to emerge. Here, we discuss a novel mechanism that contributes to mtp53’s Gain of Functions GOF (gain-of-function) activities and involves the upregulation of both nucleotide de novo synthesis and nucleoside salvage pathways. View Full-Text
Keywords: p53; nucleotide metabolism; GOFs; ETS2 p53; nucleotide metabolism; GOFs; ETS2

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Schmidt, V.; Nagar, R.; Martinez, L.A. Control of Nucleotide Metabolism Enables Mutant p53’s Oncogenic Gain-of-Function Activity. Int. J. Mol. Sci. 2017, 18, 2759.

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