共 54 条
Role of mammalian Mre11 in classical and alternative nonhomologous end joining
被引:270
作者:

Xie, Anyong
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机构:
Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA

Kwok, Amy
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机构: Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA

Scully, Ralph
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h-index: 0
机构: Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA
机构:
[1] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA
关键词:
STRAND-BREAK REPAIR;
CLASS SWITCH RECOMBINATION;
DNA-DAMAGE-RESPONSE;
V(D)J RECOMBINATION;
HISTONE H2AX;
HOMOLOGOUS RECOMBINATION;
SACCHAROMYCES-CEREVISIAE;
GENOMIC INSTABILITY;
IONIZING-RADIATION;
LENGTH MAINTENANCE;
D O I:
10.1038/nsmb.1640
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
The mammalian Mre11-Rad50-Nbs1 (MRN) complex coordinates double-strand break signaling with repair by homologous recombination and is associated with the H2A.X chromatin response to double-strand breaks, but its role in nonhomologous end joining (NHEJ) is less clear. Here we show that Mre11 promotes efficient NHEJ in both wild-type and Xrcc4(-/-) mouse embryonic stem cells. Depletion of Mre11 reduces the use of microhomology during NHEJ in Xrcc4(+/+) cells and suppresses end resection in Xrcc4(-/-) cells, revealing specific roles for Mre11 in both classical and alternative NHEJ. The NHEJ function of Mre11 is independent of H2A.X. We propose a model in which both enzymatic and scaffolding functions of Mre11 cooperate to support mammalian NHEJ.
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页码:814 / U31
页数:6
相关论文
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