Opinion - Transcription - guarding the genome by sensing DNA damage

被引:194
作者
Ljungman, M [1 ]
Lane, DP
机构
[1] Univ Michigan, Sch Med, Ctr Comprehens Canc, Dept Radiat Oncol,Div Radiat & Canc Biol, Ann Arbor, MI 48109 USA
[2] Univ Michigan, Sch Publ Hlth, Dept Environm Hlth Sci, Ann Arbor, MI 48109 USA
[3] Inst Mol & Cell Biol, Singapore 138673, Singapore
[4] Univ Dundee, Dept Surg & Mol Oncol, Dundee DD1 9SY, Scotland
基金
英国生物技术与生命科学研究理事会;
关键词
D O I
10.1038/nrc1435
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Cells induce the expression of DNA-repair enzymes, activate cell-cycle checkpoints and, under some circumstances, undergo apoptosis in response to DNA-damaging agents. The mechanisms by which these cellular responses are triggered are not well understood, but there is recent evidence that the transcription machinery might be used in DNA-damage surveillance and in triggering DNA-damage responses to suppress mutagenesis. Transcription might also act as a DNA-damage dosimeter where the severity of blockage determines whether or not to induce cell death. Could transcription therefore be a potential therapeutic target for anticancer strategies?
引用
收藏
页码:727 / 737
页数:12
相关论文
共 148 条
[61]   BRCA1 associates with processive RNA polymerase II [J].
Krum, SA ;
Miranda, GA ;
Lin, CW ;
Lane, TF .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (52) :52012-52020
[62]   Lamin A/C speckles mediate spatial organization of splicing factor compartments and RNA polymerase II transcription [J].
Kumaran, RI ;
Muralikrishna, B ;
Parnaik, VK .
JOURNAL OF CELL BIOLOGY, 2002, 159 (05) :783-793
[63]   von Hippel-Lindau protein binds hyperphosphorylated large subunit of RNA polymerase II through a proline hydroxylation motif and targets it for ubiquitination [J].
Kuznetsova, AV ;
Meller, J ;
Schnell, PO ;
Nash, JA ;
Ignacak, ML ;
Sanchez, Y ;
Conaway, JW ;
Conaway, RC ;
Czyzyk-Krzeska, MF .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (05) :2706-2711
[64]   Improving cancer therapy by non-genotoxic activation of p53 [J].
Lain, S ;
Lane, D .
EUROPEAN JOURNAL OF CANCER, 2003, 39 (08) :1053-1060
[65]   Accumulating active p53 in the nucleus by inhibition of nuclear export:: A novel strategy to promote the p53 tumor suppressor function [J].
Laín, S ;
Xirodimas, D ;
Lane, DP .
EXPERIMENTAL CELL RESEARCH, 1999, 253 (02) :315-324
[66]  
Lam LT, 2001, GENOME BIOL, V2
[67]   Therapeutic exploitation of the p53 pathway [J].
Lane, DP ;
Lain, S .
TRENDS IN MOLECULAR MEDICINE, 2002, 8 (04) :S38-S42
[68]   MDM2 - arbiter of p53's destruction [J].
Lane, DP ;
Hall, PA .
TRENDS IN BIOCHEMICAL SCIENCES, 1997, 22 (10) :372-374
[69]   CANCER - P53, GUARDIAN OF THE GENOME [J].
LANE, DP .
NATURE, 1992, 358 (6381) :15-16
[70]  
Lane DP, 1999, BRIT J CANCER, V80, P1