A20 Regulation of Nuclear Factor-κB Perspectives for Inflammatory Lung Disease

被引:36
作者
Kelly, Catriona [1 ]
Shields, Michael D. [1 ]
Elborn, J. Stuart [1 ]
Schock, Bettina C. [1 ]
机构
[1] Queens Univ Belfast, Ctr Infect & Immun, Belfast BT9 7BL, Antrim, North Ireland
关键词
A20; NF-kappa B signaling; inflammatory lung disease; ZINC-FINGER PROTEIN; BRONCHIAL EPITHELIAL-CELLS; DEPENDENT GENE-EXPRESSION; GROWTH-FACTOR RECEPTOR; TGF-BETA; ENZYME A20; AIRWAY INFLAMMATION; DISTINCT MECHANISMS; MESSENGER-RNA; TNF-ALPHA;
D O I
10.1165/rcmb.2010-0339TR
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
Persistent activation of NF-kappa B is central to the pathogenesis of many inflammatory lung disorders, including cystic fibrosis, asthma, and chronic obstructive pulmonary disease. A20 is an endogenous negative regulator of NF-kappa B signaling, which has been widely described in autoimmune and inflammatory disorders, including diabetes and Crohn's disease, but which has received little attention in terms of chronic lung disorders. This review examines the existing body of research on A20 regulation of NF-kappa B signaling and details the mechanism and regulation of A20 action focusing, where possible, on pulmonary inflammation. A20 and its associated signaling molecules are highlighted as being of potential therapeutic interest for the treatment of inflammatory disorders, and a proposed model of A20 activity in inflammatory lung disease is provided.
引用
收藏
页码:743 / 748
页数:6
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