A20: linking a complex regulator of ubiquitylation to immunity and human disease

被引：418

作者：

Ma, Averil ^{[1
]}

Malynn, Barbara A. ^{[1
]}

机构：

[1] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA

来源：

NATURE REVIEWS IMMUNOLOGY | 2012年 / 12卷 / 11期

基金：

美国国家卫生研究院;

关键词：

NF-KAPPA-B; FINGER PROTEIN A20; PSORIASIS SUSCEPTIBILITY LOCI; GENOME-WIDE ASSOCIATION; RHEUMATOID-ARTHRITIS; ENZYME A20; TNFAIP3; A20; POLYUBIQUITIN-BINDING; SIGNALING PATHWAYS; FUNCTIONAL VARIANT;

D O I：

10.1038/nri3313

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

A20 (also known as TNFAIP3) is a potent anti-inflammatory signalling molecule that restricts multiple intracellular signalling cascades. Recent studies in three general areas have converged to highlight the clinical and biological importance of A20. First, human genetic studies have strongly linked polymorphisms and mutations in the gene encoding A20 to inflammatory, autoimmune and malignant diseases. Second, studies in gene-targeted mice have revealed that A20 regulates multiple immune cell functions and prevents experimental diseases that closely mimic human conditions. Third, biochemical studies have unveiled complex mechanisms by which A20 regulates ubiquitin-dependent nuclear factor-kappa B and cell-survival signals. Taken together, these studies are revealing the importance of A20-mediated regulation of ubiquitin-dependent signalling in human disease.

引用

页码：774 / 785

页数：12

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