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. Author manuscript; available in PMC: 2014 Oct 22.
Published in final edited form as: Subcell Biochem. 2014;85:337–358. doi: 10.1007/978-94-017-9211-0_18

Figure 4. Mutant p53 can contribute to carcinogenesis via gain-of-function mechanism.

Figure 4

Hot-spot p53 mutants can regulate metabolism, suppress mitochondrial respiration, stimulate ROS production and protect against anti-cancer therapy. These activities are mediated by an interaction with different transcription factors such as: SREBP, critical for activation of mevalonate pathway, as well as NRF2 and Tap73, involved in control of mitochondrial respiration and antioxidant defense. Mutant p53 can also activate the promoter of the dUTPase gene, inducing the expression of enzyme dUTPase which suppresses therapeutic effects of fluoropyrimidine anticancer drugs.