Genomic instability, aging, and cellular senescence

被引：40

作者：

Busuttil, RA

Dollé, M

Campisi, J

Vijg, J ^{[1
]}

机构：

[1] Univ Texas, Hlth Sci Ctr, Sam & Ann Barshop Ctr Longev & Aging Studies, San Antonio, TX 78245 USA

[2] Buck Inst Age Res, Novato, CA 94945 USA

[3] Univ Calif Berkeley, Lawrence Berkeley Lab, Div Life Sci, Berkeley, CA 94720 USA

[4] S Texas Vet Hlth Care Syst, Geriatr Res Educ & Clin Ctr, San Antonio, TX 78229 USA

来源：

STRATEGIES FOR ENGINEERED NEGLIGIBLE SENESCENCE: WHY GENUINE CONTROL OF AGING MAY BE FORESEEABLE | 2004年 / 1019卷

关键词：

aging; cancer; oxidative damage; DNA damage; genomic integrity;

D O I：

10.1196/annals.1297.041

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：

Aging can be defined in practical terms as a series of time-related processes that ultimately bring life to a close. Genomic instability has been implicated as a major causal factor in aging. Here, we describe the use of a transgenic mouse model, harboring lacZ reporter genes as part of a plasmid construct integrated at one or more chromosomal locations, to study genomic instability during aging of different mouse organs and tissues as well as in mouse embryonic flbroblasts during primary culture.

引用

页码：245 / 255

页数：11

共 37 条

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