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GMEB1是一种新型内源性半胱天冬酶抑制剂,可预防缺氧和氧化应激诱导的神经元凋亡。

GMEB1, a novel endogenous caspase inhibitor, prevents hypoxia- and oxidative stress-induced neuronal apoptosis.

作者信息

Nakagawa Tadashi, Tsuruma Kazuhiro, Uehara Takashi, Nomura Yasuyuki

机构信息

Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo 060-0812, Japan.

出版信息

Neurosci Lett. 2008 Jun 13;438(1):34-7. doi: 10.1016/j.neulet.2008.04.023. Epub 2008 Apr 11.

Abstract

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.

摘要

糖皮质激素调节元件结合蛋白1(GMEB1)与前半胱天冬酶-2、-8或-9的相互作用可防止半胱天冬酶寡聚化和成熟。在本研究中,我们检测了GMEB1对缺氧和氧化应激诱导的神经元凋亡的影响。GMEB1有效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激活和凋亡,表明它作为氧化应激反应中半胱天冬酶激活和凋亡的有效抑制剂发挥作用。我们提出GMEB1可阻断由多种应激诱导的促凋亡信号。

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