Aging and genome maintenance: Lessons from the mouse?

被引：444

作者：

Hasty, P ^{[1
]}

Campisi, J

Hoeijmakers, J

van Steeg, H

Vijg, J

机构：

[1] Univ Texas, Hlth Sci Ctr, Dept Mol Med, San Antonio, TX 78245 USA

[2] Univ Texas, Hlth Sci Ctr, Dept Physiol, San Antonio, TX 78245 USA

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

[4] Lawrence Berkeley Natl Lab, Div Life Sci, Berkeley, CA 94720 USA

[5] Buck Inst Age Res, Novato, CA USA

[6] Erasmus Univ, Dept Cell Biol & Genet, CBG, NL-3000 DR Rotterdam, Netherlands

[7] Natl Inst Publ Hlth & Environm, NL-3720 BA Bilthoven, Netherlands

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

来源：

SCIENCE | 2003年 / 299卷 / 5611期

关键词：

D O I：

10.1126/science.1079161

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Recent progress in the science of aging is driven largely by the use of model systems, ranging from yeast and nematodes to mice. These models have revealed conservation in genetic pathways that balance energy production and its damaging by-products with pathways that preserve somatic maintenance. Maintaining genome integrity has emerged as a major factor in longevity and cell viability. Here we discuss the use of mouse models with defects in genome maintenance for understanding the molecular basis of aging in humans.

引用

页码：1355 / 1359

页数：5

共 55 条

[1] DNA double-strand break repair proteins are required to cap the ends of mammalian chromosomes [J].

Bailey, SM ;

Meyne, J ;

Chen, DJ ;

Kurimasa, A ;

Li, GC ;

Lehnert, BE ;

Goodwin, EH .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (26) :14899-14904

[2] Components of the Ku-dependent non-homologous end-joining pathway are involved in telomeric length maintenance and telomeric silencing [J].

Boulton, SJ ;

Jackson, SP .

EMBO JOURNAL, 1998, 17 (06) :1819-1828

[3] Cellular senescence as a tumor-suppressor mechanism [J].

Campisi, J .

TRENDS IN CELL BIOLOGY, 2001, 11 (11) :S27-S31

[4]

CAMPISI J, UNPUB

[5] p53 deficiency rescues the adverse effects of telomere loss and cooperates with telomere dysfunction to accelerate carcinogenesis [J].

Chin, L ;

Artandi, SE ;

Shen, Q ;

Tam, A ;

Lee, SL ;

Gottlieb, GJ ;

Greider, CW ;

DePinho, RA .

CELL, 1999, 97 (04) :527-538

[6]

Cooper MP, 2000, GENE DEV, V14, P907

[7] Premature aging in mice deficient in DNA repair and transcription [J].

de Boer, J ;

Andressoo, JO ;

de Wit, J ;

Huijmans, J ;

Beems, RB ;

van Steeg, H ;

Weeda, G ;

van der Horst, GTJ ;

van Leeuwen, W ;

Themmen, APN ;

Meradji, M ;

Hoeijmakers, JHJ .

SCIENCE, 2002, 296 (5571) :1276-1279

[8] The age of cancer [J].

DePinho, RA .

NATURE, 2000, 408 (6809) :248-254

[9] INCREASED SUSCEPTIBILITY TO ULTRAVIOLET-B AND CARCINOGENS OF MICE LACKING THE DNA EXCISION-REPAIR GENE XPA [J].

DEVRIES, A ;

VANOOSTROM, CTM ;

HOFHUIS, FMA ;

DORTANT, PM ;

BERG, RJW ;

DEGRUIJL, FR ;

WESTER, PW ;

VANKREIJL, CF ;

CAPEL, PJA ;

VANSTEEG, H ;

VERBEEK, SJ .

NATURE, 1995, 377 (6545) :169-173

[10] Genome dynamics in aging mice [J].

Dollé, MET ;

Vijg, J .

GENOME RESEARCH, 2002, 12 (11) :1732-1738

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