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

来源：

NATURE REVIEWS CANCER | 2004年 / 4卷 / 09期

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

页码：727 / 737

页数：12

共 148 条

[1] BRCA1 expression restores radiation resistance in BRCA1-defective cancer cells through enhancement of transcription-coupled DNA repair [J].

Abbott, DW ;

Thompson, ME ;

Robinson-Benion, C ;

Tomlinson, G ;

Jensen, RA ;

Holt, JT .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (26) :18808-18812

[2] Cell cycle checkpoint signaling through the ATM and ATR kinases [J].

Abraham, RT .

GENES & DEVELOPMENT, 2001, 15 (17) :2177-2196

[3] Transcription abnormalities potentiate apoptosis of normal human fibroblasts [J].

Andera, L ;

Wasylyk, B .

MOLECULAR MEDICINE, 1997, 3 (12) :852-863

[4] Stress signals utilize multiple pathways to stabilize p53 [J].

Ashcroft, M ;

Taya, Y ;

Vousden, KH .

MOLECULAR AND CELLULAR BIOLOGY, 2000, 20 (09) :3224-3233

[5] DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation [J].

Bakkenist, CJ ;

Kastan, MB .

NATURE, 2003, 421 (6922) :499-506

[6] The Werner syndrome protein is involved in RNA polymerase II transcription [J].

Balajee, AS ;

Machwe, A ;

May, A ;

Gray, MD ;

Oshima, J ;

Martin, GM ;

Nehlin, JO ;

Brosh, R ;

Orren, DK ;

Bohr, VA .

MOLECULAR BIOLOGY OF THE CELL, 1999, 10 (08) :2655-2668

[7] Functional interactions and signaling properties of mammalian DNA mismatch repair proteins [J].

Bellacosa, A .

CELL DEATH AND DIFFERENTIATION, 2001, 8 (11) :1076-1092

[8] NUCLEOLAR CHANGES AFTER MICROINJECTION OF ANTIBODIES TO RNA POLYMERASE-I INTO THE NUCLEUS OF MAMMALIAN-CELLS [J].

BENAVENTE, R ;

REIMER, G ;

ROSE, KM ;

HUGLEDORR, B ;

SCHEER, U .

CHROMOSOMA, 1988, 97 (02) :115-123

[9] Evidence implicating Ku antigen as a structural factor in RNA polymerase II-mediated transcription [J].

Bertinato, J ;

Tomlinson, JJ ;

Schild-Poulter, C ;

Haché, RJG .

GENE, 2003, 302 (1-2) :53-64

[10] Lack of functional pRb results in attenuated recovery of mRNA synthesis and increased apoptosis following UV radiation in human breast cancer cells [J].

Billecke, CA ;

Ljungman, ME ;

McKay, BC ;

Rehemtulla, A ;

Taneja, N ;

Ethier, SP .

ONCOGENE, 2002, 21 (29) :4481-4489

← 1 2 3 4 5 6 7 8 9 10 →