DNA repair is crucial for maintaining hematopoietic stem cell function

被引：56

作者：

Niedernhofer, Laura J. ^{[1
]}

机构：

[1] Univ Pittsburgh, Sch Med, Dept Mol Genet & Biochem, Inst Canc,Hillman Canc Ctr, Pittsburgh, PA 15213 USA

来源：

DNA REPAIR | 2008年 / 7卷 / 03期

关键词：

aging; progeria; oxidative stress; endogenous damage;

D O I：

10.1016/j.dnarep.2007.11.012

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

Richard Cornall and collaborators recently developed a mouse model of Ligase IV syndrome with growth retardation and immunodeficiency due to a defect in nonhomologous end-joining (NHEJ) of DNA double-strand breaks. They demonstrated age-dependent loss of hematopoietic stem cell function in these mice. Simultaneously, Irving Weissman and colleagues demonstrated a similar phenomenon in Ku80(-/-) mice defective in NHEJ and telomere maintenance, Xpd(TTD) mice defective in nucleotide excision repair, and late generation mTr(-/-) missing telomerase activity. These studies strongly support the hypothesis that genomic stress causes aging by limiting the ability of stem cells to indefinitely maintain tissue homeostasis. (c) 2007 Elsevier B.V. All rights reserved.

引用

页码：523 / 529

页数：7

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