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Mechanism of DNA double-strand break repair by non-homologous end joining
被引:242
作者:
Hefferin, ML
Tomkinson, AE
机构:
[1] Univ Maryland, Sch Med, Radiat Oncol Res Lab, Dept Radiat Oncol, Baltimore, MD 21201 USA
[2] Univ Maryland, Sch Med, Greenebaum Canc Ctr, Baltimore, MD 21201 USA
[3] Univ Maryland, Grad Sch, Mol & Cell Biol Grad Program, Baltimore, MD 21201 USA
来源:
关键词:
double-strand break;
non-homologous;
DNA;
D O I:
10.1016/j.dnarep.2004.12.005
中图分类号:
Q3 [遗传学];
学科分类号:
071007 ;
090102 ;
摘要:
The repair of DNA double-strand breaks (DSBs) is critical for maintaining genome stability. Although the non-homologous end joining (NHEJ) pathway frequently results in minor changes in DNA sequence at the break site and occasionally the joining of previously unlinked DNA molecules, it is a major contributor to cell survival following exposure of mammalian cells to agents that cause DSBs. This repair mechanism is conserved in lower eukaryotes and in some prokaryotes although the majority of DSBs are repaired by recombinational repair pathways in these organisms. Here we will describe the biochemical properties of NHEJ factors from bacteria, Saccharomyces cerevisiae and mammals, and how physical and functional interactions among these factors co-ordinate the repair of DSBs. (c) 2004 Elsevier B.V. All rights reserved.
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页码:639 / 648
页数:10
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