肿瘤坏死因子α
炎症
程序性细胞死亡
NFKB1型
脂多糖
细胞生物学
生物
体内
细胞凋亡
NF-κB
癌症研究
化学
免疫学
转录因子
生物化学
基因
生物技术
作者
Eric G. Lee,David L. Boone,Sophia Chai,Shon Libby,Marcia Chien,James P. Lodolce,Averil Ma
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2000-09-29
卷期号:289 (5488): 2350-2354
被引量:1326
标识
DOI:10.1126/science.289.5488.2350
摘要
A20 is a cytoplasmic zinc finger protein that inhibits nuclear factor kappaB (NF-kappaB) activity and tumor necrosis factor (TNF)-mediated programmed cell death (PCD). TNF dramatically increases A20 messenger RNA expression in all tissues. Mice deficient for A20 develop severe inflammation and cachexia, are hypersensitive to both lipopolysaccharide and TNF, and die prematurely. A20-deficient cells fail to terminate TNF-induced NF-kappaB responses. These cells are also more susceptible than control cells to undergo TNF-mediated PCD. Thus, A20 is critical for limiting inflammation by terminating TNF-induced NF-kappaB responses in vivo.
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