p53 is a tumor suppressor protein whose key function is to maintain the integrity of the cell. Mutations in p53 have been found in up to 50 % of all human cancers and cause an increase in oncogenic phenotypes such as proliferation and tumorigenicity. Both wild-type and mutant p53 have been shown to transactivate their target genes, either through directly binding to DNA, or indirectly through protein-protein interactions. This review discusses possible mechanisms behind both wild-type and mutant p53-mediated transactivation and touches on the concept of addiction to mutant p53 of cancer cells and how that may be used for future therapies.
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CITATION STYLE
Vaughan, C., Pearsall, I., Yeudall, A., Deb, S. P., & Deb, S. (2014). p53: Its mutations and their impact on transcription. Sub-Cellular Biochemistry, 85, 71–90. https://doi.org/10.1007/978-94-017-9211-0_4