OTULIN deficiency causes auto-inflammatory syndrome

被引：0

作者：

Berthe Katrine Fiil

Mads Gyrd-Hansen

机构：

[1] Ludwig Institute for Cancer Research,Nuffield Department of Medicine

[2] University of Oxford,undefined

来源：

Cell Research | 2016年 / 26卷

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摘要：

Ubiquitin chains assembled via the N-terminal methionine (Met1 or linear ubiquitin), conjugated by the linear ubiquitin chain assembly complex (LUBAC), participate in NF-κΒ-dependent inflammatory signaling and immune responses. A recent report in Cell finds that OTULIN, a deubiquitinase that selectively cleaves Met1-linked ubiquitin chains, is essential for restraining inflammation in vivo.

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页码：1176 / 1177

页数：1

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