Nitric oxide evoked p53-accumulation and apoptosis

被引：37

作者：

Brüne, B ^{[1
]}

Schneiderhan, N ^{[1
]}

机构：

[1] Univ Kaiserslautern, Fac Biol, Dept Cell Biol, D-67663 Kaiserslautern, Germany

来源：

TOXICOLOGY LETTERS | 2003年 / 139卷 / 2-3期

关键词：

radical formation; cell death; pathways of cell demise; p53;

D O I：

10.1016/S0378-4274(02)00426-5

中图分类号：

R99 [毒物学（毒理学）];

学科分类号：

100405 ;

摘要：

The tumor suppressor p53 accumulates under conditions of cellular stress and affects cell cycle progression and/or apoptosis. This has been exemplified for endogenously produced or exogenously supplied nitric oxide (NO) and thus accounts at least in part for cell destructive signaling qualities of this bioactive molecule and/or derived reactive nitrogen species. However, detailed mechanisms of toxicity and pathways of cell demise remain to be elucidated. Establishing that NO-treatment left the ubiquitination and the p53-Mdm2 interaction intact may point to an impaired nuclear-cytoplasmic shuttling to account for p53 stabilization. This was verified by heterokaryon analysis. We conclude that attenuated nuclear export contributes to stabilization and activation of p53 under the influence of NO. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：119 / 123

页数：5

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