Stimulation of polyomavirus DNA replication by wild-type p53 through the DNA-binding site.
AUTOR(ES)
Kanda, T
RESUMO
The tumor suppressor p53 possesses characteristics of a transcription factor; it binds to specific DNA sequences and activates transcription from various promoters. Here we found that murine wild-type p53 stimulated not only transcription but also polyomavirus (Py) DNA replication in a sequence-dependent manner. Oncogenic mutant p53, lacking the DNA-binding activity, showed no stimulation of Py DNA replication. Deletion of the N-terminal acidic transactivation domain of wild-type p53, which completely eliminated the ability to stimulate transcription, only impaired the function to stimulate Py DNA replication. The replication-stimulating activity of wild-type p53 was impaired by the deletion of the C-terminal oligomerization domain as well, without affecting the ability to stimulate transcription. The region responsible for the sequence-specific DNA-binding activity mapped to the central portion of the p53 molecule has a minimal activity. The results indicate that both the N-terminal and the C-terminal regions significantly contribute to the p53-mediated stimulation of Py DNA replication.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=358632Documentos Relacionados
- Interaction of p53 with its consensus DNA-binding site.
- Negative feedback regulation of wild-type p53 biosynthesis.
- Inactivation of wild-type p53 tumor suppressor by electrophilic prostaglandins
- Modulation of MDR/MRP by wild-type and mutant p53
- Wild-type p53 binds to the TATA-binding protein and represses transcription.
