Cellular responses to DNA damage

被引:423
作者
Norbury, CJ [1 ]
Hickson, ID [1 ]
机构
[1] Univ Oxford, John Radcliffe Hosp, Inst Mol Med, Imperial Canc Res Fund Labs, Oxford OX3 9DS, England
关键词
DNA damaging agents; DNA repair; genome instability; cell cycle checkpoints; apoptosis;
D O I
10.1146/annurev.pharmtox.41.1.367
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Cells are constantly under threat from the cytotoxic and mutagenic effects of DNA damaging agents. These agents can either be exogenous or formed within cells. Environmental DNA-damaging agents include UV light and ionizing radiation, as well as a variety of chemicals encountered in foodstuffs, or as air- and water-borne agents. Endogenous damaging agents include methylating species and the reactive oxygen species that arise during respiration. Although diverse responses are elicited in cells following DNA damage, this review focuses on three aspects: DNA repair mechanisms, cell cycle checkpoints, and apoptosis. Because the areas of nucleotide excision repair and mismatch repair have been covered extensively in recent reviews (1-6), we restrict our coverage of the DNA repair field to base excision repair and DNA double-strand break repair.
引用
收藏
页码:367 / 401
页数:35
相关论文
共 218 条
[1]   MRT-2 checkpoint protein is required for germline immortality and telomere replication in C-elegans [J].
Ahmed, S ;
Hodgkin, J .
NATURE, 2000, 403 (6766) :159-164
[2]   ES cells do not activate p53-dependent stress responses and undergo p53-independent apoptosis in response to DNA damage [J].
Aladjem, MI ;
Spike, BT ;
Rodewald, LW ;
Hope, TJ ;
Klemm, M ;
Jaenisch, R ;
Wahl, GM .
CURRENT BIOLOGY, 1998, 8 (03) :145-155
[3]   Cloning and characterization of a functional human homolog of Escherichia coli endonuclease III [J].
Aspinwall, R ;
Rothwell, DG ;
RoldanArjona, T ;
Anselmino, C ;
Ward, CJ ;
Cheadle, JP ;
Sampson, JR ;
Lindahl, T ;
Harris, PC ;
Hickson, ID .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (01) :109-114
[4]   ESCHERICHIA-COLI MUTY GENE-PRODUCT IS REQUIRED FOR SPECIFIC A-G-]C.G MISMATCH CORRECTION [J].
AU, KG ;
CABRERA, M ;
MILLER, JH ;
MODRICH, P .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1988, 85 (23) :9163-9166
[5]   ESCHERICHIA-COLI MUTY GENE ENCODES AN ADENINE GLYCOSYLASE ACTIVE ON G-A MISPAIRS [J].
AU, KG ;
CLARK, S ;
MILLER, JH ;
MODRICH, P .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (22) :8877-8881
[6]   Purification, characterization, gene cloning, and expression of Saccharomyces cerevisiae redoxyendonuclease, a homolog of Escherichia coli endonuclease III [J].
Augeri, L ;
Lee, YM ;
Barton, AB ;
Doetsch, PW .
BIOCHEMISTRY, 1997, 36 (04) :721-729
[7]  
Azzam EI, 1997, CELL GROWTH DIFFER, V8, P1161
[8]   Repression of CDK1 and other genes with CDE and CHR promoter elements during DNA damage-induced G2/M arrest in human cells [J].
Badie, C ;
Itzhaki, JE ;
Sullivan, MJ ;
Carpenter, AJ ;
Porter, ACG .
MOLECULAR AND CELLULAR BIOLOGY, 2000, 20 (07) :2358-2366
[9]   Targeted disruption of the gene encoding DNA ligase IV leads to lethality in embryonic mice [J].
Barnes, DE ;
Stamp, G ;
Rosewell, I ;
Denzel, A ;
Lindahl, T .
CURRENT BIOLOGY, 1998, 8 (25) :1395-1398
[10]   SITE-DIRECTED MUTAGENESIS OF THE HUMAN DNA-REPAIR ENZYME HAP1 - IDENTIFICATION OF RESIDUES IMPORTANT FOR AP ENDONUCLEASE AND RNASE-H ACTIVITY [J].
BARZILAY, G ;
WALKER, LJ ;
ROBSON, CN ;
HICKSON, ID .
NUCLEIC ACIDS RESEARCH, 1995, 23 (09) :1544-1550