Failure to regulate TNF-induced NF-κB and cell death responses in A20-deficient mice
Failure to regulate TNF-induced NF-κB and cell death responses in A20-deficient mice
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DOI：
10.1126/science.289.5488.2350
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发表时间：
2000-09-29
期刊：
影响因子：
56.9
通讯作者：
Ma, A
中科院分区：
文献类型：
--
作者：
Lee, EG;Boone, DL;Ma, A
A20是一种细胞质锌指蛋白，可抑制核因子-kappaB(NF-kappa B)活性和肿瘤坏死因子(TNF)介导的程序性细胞死亡(PCD)。肿瘤坏死因子显著增加所有组织中A20信使RNA的表达。缺乏FAR A20的小鼠会出现严重的炎症和恶病质，对脂多糖和肿瘤坏死因子都高度敏感，并过早死亡。A20缺陷细胞不能终止肿瘤坏死因子诱导的核因子-kappaB反应。这些细胞也比对照细胞更容易发生肿瘤坏死因子介导的PCD。因此，AZO在体内通过终止肿瘤坏死因子诱导的核因子-kappaB反应来限制炎症是至关重要的。
A20 is a cytoplasmic zinc finger protein that inhibits nuclear factor kappa B (NF-kappa B) activity and tumor necrosis factor (TNF)-mediated programmed cell death (PCD). TNF dramatically increases A20 messenger RNA expression in all tissues. Mice deficient far 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-kappa B responses. These cells are also more susceptible than control cells to undergo TNF-mediated PCD. Thus, AZO is critical for limiting inflammation by terminating TNF-induced NF-kappa B responses in vivo.