Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, United States.
Curr Opin Immunol. 2013 Feb;25(1):4-12. doi: 10.1016/j.coi.2012.12.005. Epub 2013 Jan 8.
The nuclear factor κ enhancer binding protein (NF-κB) family of transcription factors regulates the expression of a large array of genes involved in diverse cellular processes including inflammation, immunity and cell survival. Activation of NF-κB requires ubiquitination, a highly conserved and versatile modification that can regulate cell signaling through both proteasome dependent and independent mechanisms. Studies in the past few years have provided new insights into the mechanisms underlying regulation of NF-κB by ubiquitination, including the involvement of multiple linkages of ubiquitin, the essential role of ubiquitin binding, and the function of unanchored polyubiquitin chains. In this review, we will focus on recent advances in understanding the role of ubiquitination in NF-κB regulation in various pathways.
核因子κ增强子结合蛋白 (NF-κB) 家族转录因子调节涉及多种细胞过程的大量基因的表达，包括炎症、免疫和细胞存活。NF-κB 的激活需要泛素化，这是一种高度保守和多功能的修饰，可通过依赖和不依赖蛋白酶体的机制调节细胞信号转导。过去几年的研究为泛素化调节 NF-κB 的机制提供了新的见解，包括泛素的多种连接、泛素结合的重要作用以及无锚定多泛素链的功能。在这篇综述中，我们将重点介绍在理解泛素化在各种途径中调节 NF-κB 方面的最新进展。
