Effects of p21 deletion in mouse models of premature aging

被引：12

作者：

Benson, Erica K. ^{[1
]}

Zhao, Bo ^{[1
]}

Sassoon, David A. ^{[2
]}

Lee, Sam W. ^{[3
,4
]}

Aaronson, Stuart A. ^{[1
]}

机构：

[1] Mt Sinai Sch Med, Dept Oncol Sci, New York, NY 10029 USA

[2] Univ Paris 06, INSERM, UMR S 787, Myol Grp, Paris, France

[3] Harvard Univ, Sch Med, Charlestown, MA USA

[4] Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA USA

来源：

CELL CYCLE | 2009年 / 8卷 / 13期

关键词：

p21; premature aging; cellular senescence; tumorigenesis; Ku80; ATM; TERC; ATM-DEFICIENT MICE; CELLULAR SENESCENCE; LIFE-SPAN; REPLICATIVE SENESCENCE; HUMAN-CELLS; ATAXIA-TELANGIECTASIA; TELOMERE DYSFUNCTION; GENOME STABILITY; DNA-REPAIR; P53;

D O I：

10.4161/cc.8.13.8997

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

An approach to investigate the role of cellular senescence in organismal aging has been to abrogate signaling pathways known to induce cellular senescence and to assess the effects in mouse models of premature aging. Recently, we reported the effect of loss of function of p21, a gene implicated in p53-induced cellular senescence, in the background of the Ku80(-/-) premature aging mouse (Zhao et al., EMBO Rep 2009). Here, we provide an overview of the effects of p21 deletion in different models of premature aging.

引用

页码：2002 / 2004

页数：3

共 59 条

[1]

[Anonymous], 1962, TIME CELLS AND AGING

[2] Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice [J].

Artandi, SE ;

Chang, S ;

Lee, SL ;

Alson, S ;

Gottlieb, GJ ;

Chin, L ;

DePinho, RA .

NATURE, 2000, 406 (6796) :641-645

[3] 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

[4] Atm-deficient mice: A paradigm of ataxia telangiectasia [J].

Barlow, C ;

Hirotsune, S ;

Paylor, R ;

Liyanage, M ;

Eckhaus, M ;

Collins, F ;

Shiloh, Y ;

Crawley, JN ;

Ried, T ;

Tagle, D ;

WynshawBoris, A .

CELL, 1996, 86 (01) :159-171

[5] Partial rescue of the prophase I defects of Atm-deficient mice by p53 and p21 null alleles [J].

Barlow, C ;

Liyanage, M ;

Moens, PB ;

Deng, CX ;

Ried, T ;

WynshawBoris, A .

NATURE GENETICS, 1997, 17 (04) :462-466

[6] Atm selectively regulates distinct p53-dependent cell-cycle checkpoint and apoptotic pathways [J].

Barlow, C ;

Brown, KD ;

Deng, CX ;

Tagle, DA ;

WynshawBoris, A .

NATURE GENETICS, 1997, 17 (04) :453-456

[7] Telomeres and human disease: Ageing, cancer and beyond [J].

Blasco, MA .

NATURE REVIEWS GENETICS, 2005, 6 (08) :611-622

[8] Telomere shortening and tumor formation by mouse cells lacking telomerase RNA [J].

Blasco, MA ;

Lee, HW ;

Hande, MP ;

Samper, E ;

Lansdorp, PM ;

DePinho, RA ;

Greider, CW .

CELL, 1997, 91 (01) :25-34

[9] Bypass of senescence after disruption of p21(CIP1/WAF1) gene in normal diploid human fibroblasts [J].

Brown, JP ;

Wei, WY ;

Sedivy, JM .

SCIENCE, 1997, 277 (5327) :831-834

[10]

Campisi J, 2001, TRENDS CELL BIOL, V11, pS27, DOI 10.1016/S0962-8924(01)82148-6

← 1 2 3 4 5 6 →