OTULIN in NF-KB signaling, cell death, and disease

被引：127

作者：

Verboom, Lien ^{[1
,2
,3
]}

Hoste, Esther ^{[1
,2
,3
]}

Loo, Geert van ^{[1
,2
,3
]}

机构：

[1] VIB, Ctr Inflammat Res, B-9052 Ghent, Belgium

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

[3] Canc Res Inst Ghent CRIG, B-9000 Ghent, Belgium

来源：

TRENDS IN IMMUNOLOGY | 2021年 / 42卷 / 07期

关键词：

MEDIATED LINEAR UBIQUITINATION; SPATA2 LINKS CYLD; KAPPA-B; MET1-LINKED UBIQUITIN; LUBAC; INFLAMMATION; COMPLEX; HOIP; SHARPIN; DOMAIN;

D O I：

10.1016/j.it.2021.05.003

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Tight control of inflammatory signaling pathways is an absolute requirement to avoid chronic inflammation and disease. One of the proteins responsible for such control is OTU deubiquitinase with linear linkage specificity (OTULIN), the only mammalian deubiquitinating enzyme (DUB) exclusively hydrolyzing linear ubiquitin chains from proteins modified by the linear ubiquitin chain assembly complex (LUBAC) described thus far. Recent findings show that loss-of-function mutations in OTULIN underlie a severe early-onset human autoinflammatory disease and severe pathology in experimental mouse models. Here, we review the molecular and cellular mechanisms by which OTULIN controls inflammation and discuss the involvement of OTULIN in inflammatory disease development. We also highlight several newly identified roles for OTULIN, including a ubiquitinindependent function.

引用

页码：590 / 603

页数：14

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