PARP-1, a determinant of cell survival in response to DNA damage

被引：310

作者：

Bouchard, WJ ^{[1
]}

Rouleau, M ^{[1
]}

Poirier, GG ^{[1
]}

机构：

[1] Univ Laval, Med Res Ctr, CHUQ, Fac Med,Hlth & Environm Unit, Quebec City, PQ G1V 4G2, Canada

来源：

EXPERIMENTAL HEMATOLOGY | 2003年 / 31卷 / 06期

关键词：

BASE EXCISION-REPAIR; HUMAN POLY(ADP-RIBOSE) POLYMERASE; WILD-TYPE P53; II-DEPENDENT TRANSCRIPTION; ADP-RIBOSYLATION; AUTOMODIFICATION DOMAIN; ATAXIA-TELANGIECTASIA; CHROMATIN STRUCTURE; RIBOSE POLYMERASE; MOUSE FIBROBLASTS;

D O I：

10.1016/S0301-472X(03)00083-3

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Poly(ADP-ribose) polymerase-1 (PARP-1) plays a primary role in the process of poly(ADP-ribosyl)ation. This posttranslational modification of nuclear proteins is activated in response to DNA damage. Having been studied for more than 30 years, PARP-1 is now known to be implicated in several crucial cellular processes: DNA replication, transcription, DNA repair, apoptosis, and genome stability. In this review, we focus on recent findings suggesting that PARP-1 participates in DNA damage signaling in cell death. Of clinical relevance is its role in cancer therapy, irradiation, and chemotherapy, all of which may cause DNA damage and overactivate PARP-1, resulting in inflammation caused by necrosis. Therefore, we will discuss how inhibition of PARP-1 may enhance the efficiency of cancer therapy. (C) 2003 International Society for Experimental Hematology. Published by Elsevier Inc.

引用

页码：446 / 454

页数：9

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