Abstract
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.
Original language | English (US) |
---|---|
Pages (from-to) | 71-90 |
Number of pages | 20 |
Journal | Sub-Cellular Biochemistry |
Volume | 85 |
DOIs | |
State | Published - 2014 |
Externally published | Yes |
Keywords
- Gain-of-function
- Mutant p53
- Oncogenesis
- Transactivation
- Transcription
- Tumor suppressor
- p53
ASJC Scopus subject areas
- Medicine(all)