TRAF1 is a TNF inducible regulator of NF-κB activation

TRAF1 is a TNF inducible regulator of NF-κB activation
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DOI:
10.1016/s0014-5793(99)01356-3
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发表时间:
1999-10-29
期刊:
影响因子:
3.5
通讯作者:
Beyaert, R
Beyaert, R
中科院分区:
生物学3区
文献类型:
--
作者:
Carpentier, I;Beyaert, R

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肿瘤坏死因子受体 (TNFR) 相关因子 TRAF1 nas 首次被鉴定为 TNFR2 信号复合物的组成部分,与 TRAF 家族的其他成员不同,TRAF1 缺乏 N 端环指基序并具有组织特异性表达。在此,我们证明 TRAF1 的表达是由 TNF 和蛋白激酶 C (PKC) 激活剂 PMA 诱导的,而不是由白介素-1 (IL-1) 诱导的,TNF 诱导的 TRAF1 上调可能可以通过用蛋白酶体抑制剂 MG-132 预处理细胞来预防,而 PKC 抑制剂 Ro31-8220 则没有效果。有趣的是,HEK293T 中 TRAF1 的过表达完全阻止了 NF-κ B 激活诱导的 bg TNF、IL-1 或 TRAF2 或 TRAF6 的过表达。这些数据表明 TRAF1 的诱导表达可能在 NF-kappa B 信号通路中发挥负调节功能。 (C) 1999 年欧洲生化学会联合会。
Tumor necrosis factor receptor (TNFR)-associated factor TRAF1 nas first identified as a component of the TNFR2 signalling complex, Unlike the other members of the TRAF family, TRAF1 lacks the N-terminal ring finger motif and has a tissue specific expression, Here we demonstrate that expression of TRAF1 is induced by TNF and the protein kinase C (PKC) activator PMA, but not by interleukin-1 (IL-1), TNF-induced upregulation of TRAF1 could be prevented by pretreatment of the cells with the proteasome inhibitor MG-132, whereas the PKC inhibitor Ro31-8220,vas without effect. Interestingly, overexpression of TRAF1 in HEK293T completely prevented NF-kappa B activation induced bg TNF, IL-1, or overexpression of TRAF2 or TRAF6. These data suggest that inducible expression of TRAF1 may serve a negative regulatory function in NF-kappa B signalling pathways. (C) 1999 Federation of European Biochemical Societies.