Cellular UV damage responses - Functions of tumor suppressor p53

被引:161
作者
Latonen, L
Laiho, M
机构
[1] Univ Helsinki, Mol & Canc Biol Program, FIN-00014 Helsinki, Finland
[2] Univ Helsinki, Haartman Inst, FIN-00014 Helsinki, Finland
来源
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER | 2005年 / 1755卷 / 02期
基金
芬兰科学院;
关键词
p53 tumor suppressor; UV radiation; DNA damage; nucleotide excision repair; cell cycle arrest; apoptosis;
D O I
10.1016/j.bbcan.2005.04.003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
DNA damage, provoked by ultraviolet (UV) radiation, evokes a cellular damage response composed of activation of stress signaling and DNA checkpoint functions. These are translated to responses of replicative arrest, damage repair, and apoptosis aimed at cellular recovery from the damage. p53 tumor suppressor is a central stress response protein, activated by multiple endogenous and environmental insults, including UV radiation. The significance of p53 in the DNA damage responses has frequently been reviewed in the context of ionizing radiation or other double strand break (DSB)-inducing agents. Despite partly similar patterns, the molecular events following UV radiation are, however, distinct from the responses induced by DSBs and are profoundly coupled with transcriptional stress. These are illustrated, e.g., by the UV damage-specific translocations of Mdm2, promyelocytic leukemia protein, and nucleophosmin and their interactions with p53. In this review, we discuss UV damage-provoked cellular responses and the functions of p53 in damage recovery and cell death. (c) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:71 / 89
页数:19
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