ROS leads to MnSOD upregulation through ERK2 translocation and p53 activation in selenite-induced apoptosis of NB4 cells
ROS leads to MnSOD upregulation through ERK2 translocation and p53 activation in selenite-induced apoptosis of NB4 cells
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在亚硒酸盐诱导的 NB4 细胞凋亡中，ROS 通过 ERK2 易位和 p53 激活导致 MnSOD 上调
DOI：
10.1016/j.febslet.2010.03.040
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发表时间：
2010-06-03
期刊：
影响因子：
3.5
通讯作者：
Xu, Caimin
中科院分区：
文献类型：
--
作者：
Li, Zhushi;Shi, Kejian;Xu, Caimin
在我们之前发现亚硒酸钠诱导人白血病NB4细胞凋亡的基础上，我们现在发现在这一过程中，关键抗氧化酶锰超氧化物歧化酶（MnSOD）的表达显著升高。我们进一步发现活性氧（ROS），特别是超氧自由基，在亚硒酸盐诱导的MnSOD上调中起着至关重要的作用，与细胞外调节激酶（ERK）和p53密切相关。具体来说，ERK2在ROS的驱动下易位到细胞核中，在那里它直接磷酸化p53，导致p53与其抑制蛋白小鼠双分钟2 （MDM2）分离。活性p53直接介导MnSOD的表达，在ERK2易位和MnSOD上调之间起纽带作用。(C) 2010年欧洲生化学会联合会。Elsevier b.v.版权所有。
Following our previous finding that sodium selenite induces apoptosis in human leukemia NB4 cells, we now show that the expression of the critical antioxidant enzyme manganese superoxide dismutase (MnSOD) is remarkably elevated during this process. We further reveal that reactive oxygen species (ROS), especially superoxide radicals, play a crucial role in selenite-induced MnSOD upregulation, with extracellular regulated kinase (ERK) and p53 closely implicated. Specifically, ERK2 translocates into the nucleus driven by ROS, where it directly phosphorylates p53, leading to dissociation of p53 from its inhibitory protein mouse double minute 2 (MDM2). Active p53 directly mediates the expression of MnSOD, serving as the link between ERK2 translocation and MnSOD upregulation. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.