旧靶点新方法：通过翻译抑制的替代性核因子κB激活途径
Old target new approach: an alternate NF-kappaB activation pathway via translation inhibition.
作者信息
László Csaba F, Wu Shiyong
机构信息
Department of Chemistry and Biochemistry, Edison Biotechnology Institute, Ohio University, Athens, 45701, USA.
出版信息
Mol Cell Biochem. 2009 Aug;328(1-2):9-16. doi: 10.1007/s11010-009-0067-8. Epub 2009 Feb 18.
Abstract
Activation of the transcription factor NF-kappaB is a highly regulated multi-level process. The critical step during activation is the release from its inhibitor IkappaB, which as any other protein is under the direct influence of translation regulation. In this review, we summarize in detail the current understanding of the impact of translational regulation on NF-kappaB activation. We illustrate a newly developed mechanism of eIF2alpha kinase-mediated IkappaB depletion and subsequent NF-kappaB activation. We also show that the classical NF-kappaB activation pathways occur simultaneously with, and are complemented by, translational down regulation of the inhibitor molecule IkappaB, the importance of one or the other being shifted in accordance with the type and magnitude of the stressing agent or stimuli.
摘要
转录因子NF-κB的激活是一个受到高度调控的多水平过程。激活过程中的关键步骤是其抑制剂IκB的释放，而IκB与其他任何蛋白质一样，受到翻译调控的直接影响。在本综述中，我们详细总结了目前对翻译调控对NF-κB激活影响的理解。我们阐述了一种新发现的eIF2α激酶介导的IκB耗竭及随后NF-κB激活的机制。我们还表明，经典的NF-κB激活途径与抑制剂分子IκB的翻译下调同时发生并相互补充，根据应激源或刺激的类型和强度，两者的重要性会发生转移。
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