NF-kappaB activation by reactive oxygen species: fifteen years later.
NF-kappaB activation by reactive oxygen species: fifteen years later.
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DOI：
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发表时间：
2006
影响因子：
5.8
通讯作者：
G. Gloire;S. Legrand-Poels;J. Piette
中科院分区：
文献类型：
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作者：
G. Gloire;S. Legrand-Poels;J. Piette
转录因子NF-κ B在协调先天性和适应性免疫、细胞增殖、凋亡和发育中起主要作用。自从1991年发现NF-κ B可以被H（2）O（2）激活以来，一些实验室已经投入了相当大的努力来剖析这种激活的分子机制。早期的研究揭示了一种非典型的激活机制，导致IkappaB α Y 42磷酸化独立于IkappaB激酶（IKK），最近的研究结果表明，H（2）O（2）主要通过经典的IKK依赖性途径激活NF-κ B。然而，导致IKK激活的分子机制是细胞类型特异性的，将在这里介绍。在这篇综述中，我们还描述了其他ROS（HOCl和（1）O（2））和活性氮物种对NF-κ B活化的影响。最后，我们批判性地回顾了最近的数据突出的作用，活性氧在NF-κ B激活的促炎细胞因子（TNF-α和IL-1 β）和脂多糖（LPS），两个主要组成部分的先天免疫。
The transcription factor NF-kappaB plays a major role in coordinating innate and adaptative immunity, cellular proliferation, apoptosis and development. Since the discovery in 1991 that NF-kappaB may be activated by H(2)O(2), several laboratories have put a considerable effort into dissecting the molecular mechanisms underlying this activation. Whereas early studies revealed an atypical mechanism of activation, leading to IkappaBalpha Y42 phosphorylation independently of IkappaB kinase (IKK), recent findings suggest that H(2)O(2) activates NF-kappaB mainly through the classical IKK-dependent pathway. The molecular mechanisms leading to IKK activation are, however, cell-type specific and will be presented here. In this review, we also describe the effect of other ROS (HOCl and (1)O(2)) and reactive nitrogen species on NF-kappaB activation. Finally, we critically review the recent data highlighting the role of ROS in NF-kappaB activation by proinflammatory cytokines (TNF-alpha and IL-1beta) and lipopolysaccharide (LPS), two major components of innate immunity.