Modeling aging and cancer in the telomerase knockout mouse

被引：26

作者：

Chang, S ^{[1
]}

机构：

[1] MD Anderson Canc Ctr, Dept Mol Genet, Houston, TX 77030 USA

来源：

MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS | 2005年 / 576卷 / 1-2期

关键词：

mammalian; telomerase; telomere;

D O I：

10.1016/j.mrfmmm.2004.08.020

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

The telomerase deficient mouse has been invaluable in providing insights into basic questions pertaining to consequences of telomere dysfunction during aging and cancer in the context of the mammalian organism. Studies using this mouse model have demonstrated that cellular responses to telomere dysfunction are fundamentally conserved in both humans and mice, and that the tight regulation of telomere length and telomerase activity in somatic cells may be important in mediating the balance between aging and cancer. Here, I discuss the use of the telomerase null mouse for understanding the contrasting roles of telomeres and telomerase in organismal aging and cancer. (c) 2005 Elsevier B.V. All rights reserved.

引用

页码：39 / 53

页数：15

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