Structural studies on mechanisms to activate mutant p53

Hector Viadiu, Gilberto Fronza, Alberto Inga

Research output: Contribution to journalArticlepeer-review


The design of a broad-spectrum cancer drug would provide enormous clinical benefits to treat cancer patients. Most of cancerous cells have a mutation in the p53 gene that results in an inactive mutant p53 protein. For this reason, p53 is a prime target for the development of a broad-spectrum cancer drug. To provide the atomic information to rationally design a drug to recover p53 activity is the main goal of the structural studies on mutant p53. We review three mechanisms that influence p53 activity and provide information about how reactivation of mutant p53 can be achieved: stabilization of the active conformation of the DNA-binding domain of the protein, suppression of missense mutations in the DNA-binding domain by a second- site mutation, and increased transactivation.

Original languageEnglish
Pages (from-to)119-132
Number of pages14
JournalSub-Cellular Biochemistry
Publication statusPublished - 2014


  • Crystallography
  • Mutant p53
  • p53 activation
  • p53 structure
  • p53 transactivation
  • Suppression p53 missense mutations

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Cancer Research
  • Molecular Biology
  • Medicine(all)


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