Regulation of TNF-induced NF-κB activation by different cytoplasmic ubiquitination events

被引：53
|
作者：
Verhelst, Kelly [2 ]
Carpentier, Isabelle [2 ]
Beyaert, Rudi [1 ,2 ]
机构：
[1] VIB, Dept Mol Biomed Res, Unit Mol Signal Transduct Inflammat, Lab Mol Signal Transduct Inflammat, Ghent, Belgium
[2] Univ Ghent, Dept Biomed Mol Biol, B-9000 Ghent, Belgium
来源：
CYTOKINE & GROWTH FACTOR REVIEWS | 2011年 / 22卷 / 5-6期
关键词：
TNF; NF-kappa B; Ubiquitin; A20; Immunity; TUMOR-NECROSIS-FACTOR; ZINC-FINGER PROTEIN; FACTOR-ALPHA; POLYUBIQUITIN BINDING; LINEAR UBIQUITINATION; A20-BINDING INHIBITOR; CELL-DEATH; IN-VIVO; A20; CHAINS;
D O I：
10.1016/j.cytogfr.2011.11.002
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
TNF is a multifunctional cytokine that plays a key role in innate immunity by inducing the expression of a variety of genes that are involved in an inflammatory response. TNF-induced NF-kappa B activation is one of the best studied signaling pathways in mammalian cells and has recently led to a revival of research in the biology of ubiquitin. Many NF-kappa B signaling proteins are modified by specific ubiquitin ligases with different types of ubiquitin chains that are recognized by other proteins and which determine the outcome of ubiquitination. In addition, specific de-ubiquitinases make the whole process reversible. This review summarizes recent findings that have shaped our current understanding on the role of cytoplasmic ubiquitination events in the regulation of TNF-induced NF-kappa B signaling. (C) 2011 Elsevier Ltd. All rights reserved.
引用
收藏
页码：277 / 286
页数：10
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