Mouse models for ATR deficiency

被引:32
|
作者
O'Driscoll, Mark [1 ]
机构
[1] Univ Sussex, Human DNA Damage Response Disorders Grp, Genome Damage & Stabil Ctr, Brighton BN1 9RQ, E Sussex, England
基金
英国医学研究理事会;
关键词
ATM; ATR; Replicative stress; Intrauterine programming; Seckel syndrome; Ageing; Tissue homeostasis; Stem cell attrition; DNA-DAMAGE-RESPONSE; TARGETED DISRUPTION; CHROMOSOMAL FRAGMENTATION; ATAXIA-TELANGIECTASIA; CANCER-CELLS; GENE ATR; LEADS; CAFFEINE; REVEALS; UVB;
D O I
10.1016/j.dnarep.2009.09.001
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
ATM and ATR orchestrate overlapping DNA damage responses in reply to different forms of DNA strand discontinuities. But, knockout mouse models suggest that ATR is essential for viability in contrast to ATM. Recently, more sophisticated mouse models have been published including a conditional ATR-knockdown system and by modelling the human ATR-Seckel syndrome-causative mutation. Here, I will overview and contrast these models highlighting the advances both represent in our understanding of how defects in the ATR-dependent DNA damage response can impact on normal development, tissue homeostasis, ageing and cancer. (C) 2009 Elsevier B.V. All rights reserved.
引用
收藏
页码:1333 / 1337
页数:5
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