| Literature DB >> 25201189 |
Catherine Vaughan1, Isabella Pearsall, Andrew Yeudall, Swati Palit Deb, Sumitra Deb.
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.Entities:
Mesh:
Year: 2014 PMID: 25201189 DOI: 10.1007/978-94-017-9211-0_4
Source DB: PubMed Journal: Subcell Biochem ISSN: 0306-0225