DNA double-strand break repair and development

被引:39
作者
Phillips, E. R.
McKinnon, P. J.
机构
[1] St Jude Childrens Hosp, Dept Genet & Tumor Cell Biol, Memphis, TN 38105 USA
[2] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA
关键词
DNA repair; double-strand breaks; ATM; NHEJ; development;
D O I
10.1038/sj.onc.1210877
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
Normal development of an organism requires the ability to respond to DNA damage. A particularly deleterious lesion is a DNA double-strand break (DSB). The cellular response to DNA DSBs occurs via an integrated sensing and signaling network that maintains genomic stability. The outcomes of defective DNA DSB repair are related to the developmental stage of an organism, and often show striking tissue specificity. Many human diseases are associated with deficiencies in DNA DSB repair and can be characterized by neuropathology, immune deficiency, growth retardation or predisposition to cancer. This review will focus on the requirements of the DNA DSB response that function to maintain homeostasis during mammalian development.
引用
收藏
页码:7799 / 7808
页数:10
相关论文
共 147 条
[1]   XLF interacts with the XRCC4-DNA ligase IV complex to promote DNA nonhomologous end-joining [J].
Ahnesorg, P ;
Smith, P ;
Jackson, SP .
CELL, 2006, 124 (02) :301-313
[2]   Involvement of poly(ADP-ribose) polymerase-1 and XRCC1/DNA ligase III in an alternative route for DNA double-strand breaks rejoining [J].
Audebert, M ;
Salles, B ;
Calsou, P .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (53) :55117-55126
[3]   DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation [J].
Bakkenist, CJ ;
Kastan, MB .
NATURE, 2003, 421 (6922) :499-506
[4]   Initiating cellular stress responses [J].
Bakkenist, CJ ;
Kastan, MB .
CELL, 2004, 118 (01) :9-17
[5]   Atm-deficient mice: A paradigm of ataxia telangiectasia [J].
Barlow, C ;
Hirotsune, S ;
Paylor, R ;
Liyanage, M ;
Eckhaus, M ;
Collins, F ;
Shiloh, Y ;
Crawley, JN ;
Ried, T ;
Tagle, D ;
WynshawBoris, A .
CELL, 1996, 86 (01) :159-171
[6]   Targeted disruption of the gene encoding DNA ligase IV leads to lethality in embryonic mice [J].
Barnes, DE ;
Stamp, G ;
Rosewell, I ;
Denzel, A ;
Lindahl, T .
CURRENT BIOLOGY, 1998, 8 (25) :1395-1398
[7]   DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis [J].
Bartkova, J ;
Horejsi, Z ;
Koed, K ;
Krämer, A ;
Tort, F ;
Zieger, K ;
Guldberg, P ;
Sehested, M ;
Nesland, JM ;
Lukas, C ;
Orntoft, T ;
Lukas, J ;
Bartek, J .
NATURE, 2005, 434 (7035) :864-870
[8]   Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints [J].
Bartkova, Jirina ;
Rezaei, Nousin ;
Liontos, Michalis ;
Karakaidos, Panagiotis ;
Kletsas, Dimitris ;
Issaeva, Natalia ;
Vassiliou, Leandros-Vassilios F. ;
Kolettas, Evangelos ;
Niforou, Katerina ;
Zoumpourlis, Vassilis C. ;
Takaoka, Munenori ;
Nakagawa, Hiroshi ;
Tort, Frederic ;
Fugger, Kasper ;
Johansson, Fredrik ;
Sehested, Maxwell ;
Andersen, Claus L. ;
Dyrskjot, Lars ;
Orntoft, Torben ;
Lukas, Jiri ;
Kittas, Christos ;
Helleday, Thomas ;
Halazonetis, Thanos D. ;
Bartek, Jiri ;
Gorgoulis, Vassilis G. .
NATURE, 2006, 444 (7119) :633-637
[9]   The cellular response to general and programmed DNA double strand breaks [J].
Bassing, CH ;
Alt, FW .
DNA REPAIR, 2004, 3 (8-9) :781-796
[10]   Dynamic assembly and sustained retention of 53BP1 at the sites of DNA damage are controlled by Mdc1/NFBD1 [J].
Bekker-Jensen, S ;
Lukas, C ;
Melander, F ;
Bartek, J ;
Lukas, J .
JOURNAL OF CELL BIOLOGY, 2005, 170 (02) :201-211