Inflammatory diseases: Is ubiquitinated NEMO at the hub?

被引：33

作者：

Burns, KA ^{[1
]}

Martinon, F ^{[1
]}

机构：

[1] Univ Lausanne, Dept Biochem, BIL Biomed Res Ctr, CH-1066 Epalinges, Switzerland

来源：

CURRENT BIOLOGY | 2004年 / 14卷 / 24期

关键词：

D O I：

10.1016/j.cub.2004.11.040

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Many patients with Crohn's disease carry mutations in NOD2, a molecule that can both activate and attenuate the pro-inflammatory effects of NF-kappaB. Recent studies implicate NOD2-induced ubiquitination of the NF-kappaB regulator NEMO as a potential means of manipulating the NF-kappaB signal.

引用

页码：R1040 / R1042

页数：3

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