Regulation of endogenous E2F1 stability by the retinoblastoma family proteins
AUTOR(ES)
Martelli, Fabio
FONTE
The National Academy of Sciences
RESUMO
Certain E2F transcription factor species play a pivotal role in regulating cell-cycle progression. The activity of E2F1, a protein with neoplastic transforming activity when unregulated, is tightly controlled at the transcriptional level during G0 exit. In addition, during this interval, the stability of endogenous E2F1 protein increased markedly. E2F1 stability also was dynamically regulated during myogenic differentiation and in response to gamma irradiation. One or more retinoblastoma family proteins likely participate in the stability process, because simian virus 40 T antigen disrupted E2F1 stability regulation during G1 exit in a manner dependent on its ability to bind to pocket proteins. Thus, endogenous E2F1 function is regulated by both transcriptional and posttranscriptional control mechanisms.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=15859Documentos Relacionados
- Regulation of E2F1 activity by acetylation
- Dual mechanisms of repression of E2F1 activity by the retinoblastoma gene product.
- Regulation of E2F1 by BRCT Domain-Containing Protein TopBP1
- Oncogenic capacity of the E2F1 gene.
- A genetic analysis of the E2F1 gene distinguishes regulation by Rb, p107, and adenovirus E4.
