NF-κB activator Act1 associates with IL-1/Toll pathway adaptor molecule TRAF6

NF-κB activator Act1 associates with IL-1/Toll pathway adaptor molecule TRAF6
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DOI:
10.1016/s0014-5793(02)03688-8
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发表时间:
2002-12-04
期刊:
影响因子:
3.5
通讯作者:
Suzuki, H
Suzuki, H
中科院分区:
生物学3区
文献类型:
--
作者:
Kanamori, M;Kai, C;Suzuki, H

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NF-kappaB激活因子1(Act 1),也称为CIKS,是最近鉴定的通过与IkappaB激酶复合物结合而具有NF-kappaB和AP-1激活活性的蛋白质。我们鉴定并证实了Act 1与肿瘤坏死因子受体相关因子6(TRAF 6)相互作用;值得注意的是,Act 1仅在TRAF家族蛋白中与TRAF 6结合。Act 1的氨基末端一半是其与TRAF结构域相互作用所必需的。Act 1介导的NF-κ B激活被TRAF 6的显性负突变体以剂量依赖性方式抑制,并且IL-1诱导的NF-κ B激活被高水平的Act 1表达抑制。我们的研究结果表明,Act 1是通过TRAF 6参与IL-1/Toll介导的信号转导。(C)2002年欧洲生物化学学会联合会。出版;由Elsevier Science B. V.保留所有权利。
NF-kappaB activator 1 (Act1), also called CIKS, is a recently identified protein with NF-kappaB and AP-1 activation activities through its association with the IkappaB kinase complex. We identified and confirmed that Act1 interacts with tumor necrosis factor receptor-associated factor 6 (TRAF6); notably, Act1 binds to TRAF6 only among TRAF family proteins. The amino-terminal half of Act1 is required for its interaction with the TRAF domain. Act1-mediated NF-kappaB activation was inhibited by a dominant-negative mutant of TRAF6 in a dose-dependent manner, and IL-1-induced NF-kappaB activation was inhibited by a high level of Act1 expression. Our results suggest that Act1 is involved in IL-1/Toll-mediated signaling through TRAF6. (C) 2002 Federation of European Biochemical Societies. Published; by Elsevier Science B.V. All rights reserved.