Fanconi anemia (cross)linked to DNA repair

被引：248
作者：
Niedernhofer, LJ
Lalai, AS
Hoeijmakers, JHJ
机构：
[1] Erasmus Med Ctr, Dept Cell Biol & Genet, Ctr Biomed Genet, Ctr Genet Med, NL-3000 DR Rotterdam, Netherlands
[2] Univ Pittsburgh, Sch Med, Dept Mol Genet & Biochem, Inst Canc, Pittsburgh, PA 15213 USA
来源：
CELL | 2005年 / 123卷 / 07期
关键词：
D O I：
10.1016/j.cell.2005.12.009
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：
Fanconi anemia is characterized by hypersensitivity to DNA interstrand crosslinks (ICLs) and susceptibility to tumor formation. Despite the identification of numerous Fanconi anemia (FANC) genes, the mechanism by which proteins encoded by these genes protect a cell from DNA interstrand crosslinks remains unclear. The recent discovery of two DNA helicases that, when defective, cause Fanconi anemia tips the balance in favor of the direct involvement of the FANC proteins in DNA repair and the bypass of DNA lesions. ©2005 Elsevier Inc.
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收藏
页码：1191 / 1198
页数：8
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