OTULIN deficiency causes auto-inflammatory syndrome

被引：0
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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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