PUBLICATION
p53/p63/p73 isoforms: an orchestra of isoforms to harmonise cell differentiation and response to stress
- Authors
- Murray-Zmijewski, F., Lane, D.P., and Bourdon, J.C.
- ID
- ZDB-PUB-060412-15
- Date
- 2006
- Source
- Cell death and differentiation 13(6): 962-972 (Review)
- Registered Authors
- Keywords
- splice, promoter, drosophila, zebrafish, development, cancer
- MeSH Terms
-
- Cell Differentiation/genetics*
- Transcription Factors
- Tumor Suppressor Proteins/genetics
- Tumor Suppressor Proteins/metabolism*
- Animals
- Cell Cycle Proteins/genetics
- Cell Cycle Proteins/metabolism
- DNA-Binding Proteins/genetics
- DNA-Binding Proteins/metabolism*
- Mutation
- Tumor Suppressor Protein p53/genetics
- Tumor Suppressor Protein p53/metabolism*
- Promoter Regions, Genetic/genetics
- Humans
- Trans-Activators/genetics
- Trans-Activators/metabolism*
- Evolution, Molecular
- DNA/genetics
- DNA/metabolism
- Nuclear Proteins/genetics
- Nuclear Proteins/metabolism*
- Alternative Splicing
- Mice, Knockout
- Apoptosis Regulatory Proteins/genetics
- Apoptosis Regulatory Proteins/metabolism
- Cell Transformation, Neoplastic/genetics
- Cell Transformation, Neoplastic/metabolism
- Neoplasms/genetics
- Neoplasms/metabolism
- Mice
- Transcription, Genetic
- Protein Isoforms/genetics
- Protein Isoforms/metabolism
- PubMed
- 16601753 Full text @ Cell Death Differ.
Citation
Murray-Zmijewski, F., Lane, D.P., and Bourdon, J.C. (2006) p53/p63/p73 isoforms: an orchestra of isoforms to harmonise cell differentiation and response to stress. Cell death and differentiation. 13(6):962-972.
Abstract
p63, p73 and p53 compose a family of transcription factors involved in cell response to stress and development. p53 is the most frequently mutated gene in cancer (50%) and loss of p53 activity is considered to be ubiquitous to all cancers. Recent publications may have a profound impact on our understanding of p53 tumour suppressor activity. p63, p73 and p53 genes have a dual gene structure conserved in drosophila, zebrafish and man. They encode for multiple p63, p73 or p53 proteins containing different protein domains (isoforms) due to multiple splicing, alternative promoter and alternative initiation of translation. In this review, we describe the different isoforms of p63, p73, p53 and their roles in development and cancer. The changes in the interactions between p53, p63 and p73 isoforms are likely to be fundamental to our understanding in the transition between normal cell cycling and the onset of tumour formation.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping