Mechanism of rescue of common p53 cancer mutations by second-site suppressor mutations.

@article{Nikolova2000MechanismOR,
  title={Mechanism of rescue of common p53 cancer mutations by second-site suppressor mutations.},
  author={Penka V. Nikolova and K B Wong and Brian S DeDecker and Julia Henckel and A. R. Fersht},
  journal={The EMBO journal},
  year={2000},
  volume={19 3},
  pages={370-8}
}
The core domain of p53 is extremely susceptible to mutations that lead to loss of function. We analysed the stability and DNA-binding activity of such mutants to understand the mechanism of second-site suppressor mutations. Double-mutant cycles show that N239Y and N268D act as 'global stability' suppressors by increasing the stability of the cancer mutants G245S and V143A-the free energy changes are additive. Conversely, the suppressor H168R is specific for the R249S mutation: despite… CONTINUE READING

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