Altered-function p53 missense mutations identified in breast cancers can have subtle effects on transactivation.

ABSTRACT: Mutations of the sequence-specific master regulator p53 that alter transactivation function from promoter response elements (RE) could result in changes in the strength of gene activation or spectra of genes regulated. Such mutations in this tumor suppressor might lead to dramatic phenotypic changes and diversification of cell responses to stress. We have determined "functional fingerprints" of sporadic breast cancer-related p53 mutants, many of which are also associated with familial cancer proneness such as the Li-Fraumeni syndrome and germline BRCA1/2 mutant-associated cancers. The ability of p53, wild-type and mutants, to transactivate from 11 human target REs has been assessed at variable expression levels using a cellular, isogenomic yeast model system that allows for the rapid analy

SUBMITTER: Jordan JJ 

PROVIDER: S-EPMC2873663 | biostudies-literature | 2010 May

REPOSITORIES: biostudies-literature