Cahill Dana, Connor Brian, Carney James P
Radiation Oncology Research Laboratory, Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
Front Biosci. 2006 May 1;11:1958-76. doi: 10.2741/1938.
For all cells, a DNA double strand break (DSB) is a dangerous lesion that can have profound consequences for the genome. If a DSB is encountered during mitosis, chromosomal separation may be adversely affected. Alternatively, during S phase a DSB may cause replication fork stalling or collapse. Improperly repaired DSBs can result in chromosomal rearrangements, senescence or activation of apoptotic pathways. Cells have developed sophisticated recombination pathways to metabolize and repair DSBs quickly as well as the capacity to differentiate physiologically occurring breaks from life threatening lesions. The two major pathways of recombination repair are known as non-homologous end-joining (NHEJ) and homologous recombination (HR). In this review, we will discuss the detection, response, and repair of DSBs in eukaryotes.
对于所有细胞而言，DNA双链断裂（DSB）是一种危险的损伤，可能会对基因组产生深远影响。如果在有丝分裂期间遇到DSB，染色体分离可能会受到不利影响。另外，在S期，DSB可能导致复制叉停滞或崩溃。修复不当的DSB会导致染色体重排、衰老或凋亡途径的激活。细胞已经发展出复杂的重组途径来快速代谢和修复DSB，以及区分生理性断裂和危及生命的损伤的能力。重组修复的两个主要途径被称为非同源末端连接（NHEJ）和同源重组（HR）。在本综述中，我们将讨论真核生物中DSB的检测、反应和修复。
