| Autor: |
Secretan MB; Department of Pathology, UCLA School of Medicine and Public Health, Los Angeles, CA, USA., Scuric Z, Oshima J, Bishop AJ, Howlett NG, Yau D, Schiestl RH |
| Jazyk: |
angličtina |
| Zdroj: |
Mutation research [Mutat Res] 2004 Oct 04; Vol. 554 (1-2), pp. 351-64. |
| DOI: |
10.1016/j.mrfmmm.2004.05.016 |
| Abstrakt: |
In mammalian cells, DNA double-strand breaks are repaired by non-homologous end-joining and homologous recombination, both pathways being essential for the maintenance of genome integrity. We determined the effect of mutations in Ku86 and DNA-PK on the efficiency and the accuracy of double-strand break repair by non-homologous end-joining and homologous recombination in mammalian cells. We used an assay, based on the transient transfection of a linearized plasmid DNA, designed to simultaneously detect transfection and recombination markers. In agreement with previous results non-homologous end-joining was largely compromised in Ku86 deficient cells, and returned to normal in the Ku86-complemented isogenic cell line. In addition, analysis of DNA plasmids recovered from Ku86 mutant cells showed an increased use of microhomologies at the nonhomologous end joining junctions, and displayed a significantly higher frequency of DNA insertions compared to control cells. On the other hand, the DNA-PKcs deficient cell lines showed efficient double-strand break repair by both mechanisms. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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