X-linked inhibitor of apoptosis protein increases mitochondrial antioxidants through NF-κB activation
X-linked inhibitor of apoptosis protein increases mitochondrial antioxidants through NF-κB activation
复制标题
DOI：
10.1016/j.bbrc.2007.09.115
复制
发表时间：
2007-12-07
影响因子：
3.1
通讯作者：
Lindholm, Dan
中科院分区：
文献类型：
--
作者：
Kairisalo, Minna;Korhonen, Laura;Lindholm, Dan
X染色体连锁的凋亡抑制蛋白是半胱氨酸天冬氨酸酶的内源性抑制蛋白，是细胞死亡的重要调节因子。XIAP也可以影响细胞信号转导，但受影响的下游蛋白在很大程度上是未知的。我们在这里使用神经元PC6.3细胞显示，XIAP增加了抗氧化剂的水平，特别是定位于线粒体的超氧化物歧化酶-2。使用报告构建体和缺乏NF-kappa B rel-A的小鼠胚胎成纤维细胞的研究表明，在XIAP诱导Sod2的过程中，需要NF-kappa B信号。XIAP还减少了PC6.3细胞的氧化应激，表现为减少了活性氧物种的产生。这些发现揭示了XIAP在控制氧化应激和线粒体抗氧化剂方面的新作用，这些抗氧化剂可能有助于在各种损伤后保护细胞。(C)2007 Elsevier Inc.保留所有权利。
X chromosome-linked inhibitor of apoptosis protein is an endogenous inhibitor of caspases and is an important regulator of cell death. XIAP can also influence cell signaling, but downstream proteins affected are largely unknown. We show here using neuronal PC6.3 cells that XIAP increases the levels of antioxidants, particularly superoxide dismutase-2 that is localized to mitochondria. Studies using reporter constructs and NF-kappa B Rel-A deficient mouse embryonic fibroblasts showed that NF-kappa B signaling is required for the induction of Sod2 by XIAP. XIAP also reduced oxidative stress in the PC6.3 cells as shown by decreased production of reactive oxygen species. These findings disclose a novel role for XIAP in control of oxidative stress and mitochondrial antioxidants that may contribute to cell protection after various injuries. (C) 2007 Elsevier Inc. All rights reserved.