Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 105, Issue 52, Pages 20689-20694Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0811241106
Keywords
-
Categories
Funding
- Centre National de la Recherche Scientifique
- Association pour la Recherche sur le Cancer
- Swiss National Science Foundation
- University of Zurich
- French Fondation pour la Recherche Medicale
- Vetsuisse Dean FR Althaus
- Associazione Italiana Ricerca sul Cancro
- Institut National de la Sante et de la Recherche Medicale
- Fondazione Cariplo [2006-0734]
- Fondazione Italiana per la Ricerca sul Cancro Fellowship
Ask authors/readers for more resources
The adenine misincorporated by replicative DNA polymerases (pols) opposite 7,8-dihydro-8-oxoguanine (8-oxo-G) is removed by a specific glycosylase, leaving the lesion on the DNA. Subsequent incorporation of C opposite 8-oxo-G on the resulting 1-nt gapped DNA is essential for the removal of the 8-oxo-G to prevent G-C to T-A transversion mutations. By using model DNA templates, purified DNA pols beta and lambda and knockout cell extracts, we show here that the auxiliary proteins replication protein A and proliferating cell nuclear antigen act as molecular switches to activate the DNA pol lambda- dependent highly efficient and faithful repair of A: 8-oxo-G mismatches in human cells and to repress DNA pol beta activity. By using an immortalized human fibroblast cell line that has the potential to induce cancer in mice, we show that the development of a tumoral phenotype in these cells correlated with a differential expression of DNA pols lambda and beta.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available