GMEB1, a novel endogenous caspase inhibitor, prevents hypoxia- and oxidative stress-induced neuronal apoptosis
GMEB1, a novel endogenous caspase inhibitor, prevents hypoxia- and oxidative stress-induced neuronal apoptosis
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DOI：
10.1016/j.neulet.2008.04.023
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发表时间：
2008-06-13
影响因子：
2.5
通讯作者：
Nomura, Yasuyuki
中科院分区：
文献类型：
--
作者：
Nakagawa, Tadashi;Tsuruma, Kazuhiro;Nomura, Yasuyuki
糖皮质激素调节元件结合蛋白1（GMEB 1）与半胱天冬酶原-2、-8或-9的相互作用阻止半胱天冬酶寡聚化和成熟。在本研究中，我们研究了GMEB 1对缺氧和氧化应激诱导的神经细胞凋亡的影响。GMEB 1有效地减弱了人神经母细胞瘤SK-N-MC细胞中由这些应激引起的半胱天冬酶活化和凋亡，表明其作为响应于氧化应激的半胱天冬酶活化和凋亡的有效抑制剂发挥作用。我们建议，GMEB 1块促凋亡信号诱导的各种压力。(C)2008爱思唯尔爱尔兰有限公司保留所有权利。
The interaction of glucocorticoid modulatory element-binding protein 1 (GMEB1) with procaspase-2, -8, or -9 prevents caspase oligomerization and maturation. In the present study, we examined the effect of GMEB1 on neuronal apoptosis induced by hypoxia and oxidative stress. GMEB1 effectively attenuated caspase activation and apoptosis caused by these stresses in human neuroblastoma SK-N-MC cells, indicating that it functions as a potent inhibitor of caspase activation and apoptosis in response to oxidative stress. We propose that GMEB1 blocks pro-apoptosis signals induced by a variety of stresses. (C) 2008 Elsevier Ireland Ltd. All rights reserved.