Mouse models of DNA double-strand break repair and neurological disease

被引：35

作者：

Frappart, Pierre-Olivier ^{[1
]}

McKinnon, Peter J. ^{[1
]}

机构：

[1] St Jude Childrens Res Hosp, Dept Genet & Tumor Cell Biol, Memphis, TN 38105 USA

来源：

DNA REPAIR | 2008年 / 7卷 / 07期

关键词：

DNA repair; double-strand breaks; homologous recombination; non-homologous end-joining; neurodegeneration; nervous system;

D O I：

10.1016/j.dnarep.2008.03.007

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

The repair of DNA damage is essential for the prevention of disease. The DNA double-strand break (DSB) is a particularly hazardous lesion. DNA DSBs activate a coordinated cellular response involving cell cycle checkpoint activation and repair of the DNA break, or alternatively apoptosis. In the nervous system the inability to respond to DNA DSBs may lead to neurodegenerative disease or brain tumors. Therefore, understanding the DNA DSB response mechanism in the nervous system is of high importance for developing new treatments for neurodegeneration and cancer. In this regard, the use of mouse models represents an important approach for advancing our understanding of the biology of the DNA damage response in the nervous system. (C) 2008 Elsevier B.V All rights reserved.

引用

页码：1051 / 1060

页数：10

共 119 条

[1] Cell cycle checkpoint signaling through the ATM and ATR kinases [J].

Abraham, RT .

GENES & DEVELOPMENT, 2001, 15 (17) :2177-2196

[2] Recruitment of ATR to sites of ionising radiation-induced DNA damage requires ATM and components of the MRN protein complex [J].

Adams, KE ;

Medhurst, AL ;

Dart, DA ;

Lakin, ND .

ONCOGENE, 2006, 25 (28) :3894-3904

[3] 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

[4] Potential role for adult neurogenesis in the encoding of time in new memories [J].

Aimone, James B. ;

Wiles, Janet ;

Gage, Fred H. .

NATURE NEUROSCIENCE, 2006, 9 (06) :723-727

[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] The cellular response to general and programmed DNA double strand breaks [J].

Bassing, CH ;

Alt, FW .

DNA REPAIR, 2004, 3 (8-9) :781-796

[8] Ascl1 defines sequentially generated lineage-restricted neuronal and oligodendrocyte precursor cells in the spinal cord [J].

Battiste, James ;

Helms, Amy W. ;

Kim, Euiseok J. ;

Savage, Trisha K. ;

Lagace, Diane C. ;

Mandyam, Chitra D. ;

Eisch, Amelia J. ;

Miyoshi, Goichi ;

Johnson, Jane E. .

DEVELOPMENT, 2007, 134 (02) :285-293

[9] Cancer predisposition and hematopoietic failure in Rad50S/S mice [J].

Bender, CF ;

Sikes, ML ;

Sullivan, R ;

Huye, LE ;

Le Beau, MM ;

Roth, DB ;

Mirzoeva, OK ;

Oltz, EM ;

Petrini, JHJ .

GENES & DEVELOPMENT, 2002, 16 (17) :2237-2251

[10] Roles of ATM and NBS1 in chromatin structure modulation and DNA double-strand break repair [J].

Berkovich, Elijahu ;

Monnat, Raymond J., Jr. ;

Kastan, Michael B. .

NATURE CELL BIOLOGY, 2007, 9 (06) :683-U137

← 1 2 3 4 5 6 7 8 9 10 →