A20 in inflammation and autoimmunity

被引：447

作者：

Catrysse, Leen ^{[1
,2
]}

Vereecke, Lars ^{[1
,2
]}

Beyaert, Rudi ^{[1
,2
]}

van Loo, Geert ^{[1
,2
]}

机构：

[1] VIB, Inflammat Res Ctr, Unit Mol Signal Transduct Inflammat, B-9052 Ghent, Belgium

[2] Univ Ghent, Dept Biomed Mol Biol, B-9052 Ghent, Belgium

来源：

TRENDS IN IMMUNOLOGY | 2014年 / 35卷 / 01期

关键词：

A20; tumor necrosis factor alpha-induced protein 3; nuclear factor-kappa B; inflammation; apoptosis; ubiquitination; NF-KAPPA-B; EDITING ENZYME A20; ZINC-FINGER PROTEIN; SYSTEMIC-LUPUS-ERYTHEMATOSUS; RHEUMATOID-ARTHRITIS; CELL-PROLIFERATION; LINEAR UBIQUITINATION; FEEDBACK INHIBITION; IMMUNE HOMEOSTASIS; NEGATIVE REGULATOR;

D O I：

10.1016/j.it.2013.10.005

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

Although known for many years as a nuclear factor (NF)-kappa B inhibitory and antiapoptotic signaling protein, A20 has recently attracted much attention because of its ubiquitin-regulatory activities and qualification by genome-wide association studies (GWASs) as a susceptibility gene for inflammatory disease. Here, we review new findings that have shed light on the molecular and biochemical mechanisms by which A20 regulates inflammatory signaling cascades, and discuss recent experimental evidence characterizing A20 as a crucial gatekeeper preserving tissue homeostasis.

引用

页码：22 / 31

页数：10

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