Recent advances towards understanding redox mechanisms in the activation of nuclear factor κB
Recent advances towards understanding redox mechanisms in the activation of nuclear factor κB
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DOI：
10.1016/s0891-5849(00)00218-5
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发表时间：
2000-05-01
影响因子：
7.4
通讯作者：
Baeuerle, PA
中科院分区：
文献类型：
--
作者：
Janssen-Heininger, YMW;Poynter, ME;Baeuerle, PA
核转录因子-kappaB(NF-kappa B)因其在免疫和炎症基因调控、细胞凋亡和细胞增殖中的重要作用而被广泛研究。核因子-kappaB是一种氧化还原敏感的转录因子，这一点早在十多年前就已为人所知。由于许多相互矛盾的报道，关于氧化还原调节的作用以及核因子-kappaB激活途径中潜在的氧化还原敏感部位的位置一直存在激烈的争论。核因子-kappa B的氧化还原调节已经在这本杂志中被广泛讨论，读者可以参考关于这个主题的两个全面的评论[1，2]。随着降解抑制剂Ikappa B附近的信号中间产物的发现，潜在的氧化还原敏感位点的数量正在迅速增加。这篇综述的目的是阐述最近对促炎症细胞因子如肿瘤坏死因子-α和白介素1-β所触发的核因子-kappa B信号转导通路的认识。此外，一氧化氮((NO)-N-.)在对核因子-kappaB的调控方面进行综述。将讨论发生在I kappa B-α降解上游的氧化还原调节机会，以及对核因子-kappa B亚单位磷酸化进行氧化还原控制的可能性。对氧化还原敏感的步骤可能取决于核因子-kappa B激活剂的性质，所涉及的活性氧或氮物种的类型，激活的信号通路的选择性，以及正在研究的细胞类型。最后，讨论了氧化还原对核因子-kappaB活化的调节可能涉及多个亚细胞室。(C)2000年爱思唯尔科学公司。
The transcription factor, nuclear factor-kappa B (NF-kappa B) has been studied extensively due to its prominent role in the regulation of immune and inflammatory genes, apoptosis, and cell proliferation. It has been known for more that a decade that NF-kappa B is a redox-sensitive transcription factor. The contribution of redox regulation and the location of potential redox-sensitive sites within the NF-kappa B activation pathway are subject to intense debate due to many conflicting reports. Redox regulation of NF-kappa B has been extensively addressed in this journal and the reader is referred to two comprehensive reviews on the subject [1,2]. With the identification of signaling intermediates proximal to the degradation of the inhibitor, I kappa B, the number of potential redox-sensitive sites is rapidly increasing. The purpose of this review is to address recent insights into the NF-kappa B signaling cascades that an triggered by proinflammatory cytokines such as TNF-alpha and IL-1 beta. In addition, the role of nitrogen monoxide ((NO)-N-.) in the regulation of NF-kappa B will be reviewed. Opportunities for redox regulation that occur upstream of I kappa B-alpha degradation, as well as the potential for redox control of phosphorylation of NF-kappa B subunits, will be discussed. Redox-sensitive steps are likely to depend on the nature of the NF-kappa B activator, the type of reactive oxygen or nitrogen species involved, the selectivity of signaling pathways activated, as well as the cell type under investigation. Lastly, it is discussed how redox regulation of NF-kappa B activation is likely to involve multiple subcellular compartments. (C) 2000 Elsevier Science Inc.