Involvement of GSK-3β in TWEAK-mediated NF-κB activation
Involvement of GSK-3β in TWEAK-mediated NF-κB activation
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DOI：
10.1016/j.febslet.2004.04.041
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发表时间：
2004-05-21
期刊：
影响因子：
3.5
通讯作者：
Moelans, I
中科院分区：
文献类型：
--
作者：
De Ketelaere, A;Vermeulen, L;Moelans, I
糖原合成酶激酶 3beta (GSK-3beta) 是多种信号转导通路的关键组成部分。我们发现“TNF 样弱凋亡诱导剂”的短变体 (shortTWEAK) 在酵母双杂交系统中与 GSK-3beta 形成复合物。我们证明，shortTWEAK 和 GSK-3beta 共定位于人神经母细胞瘤细胞的细胞核中。我们还表明，TWEAK 内化于不同的细胞系中，并易位至细胞核。该事件导致 IBα 降解、GSK-3β 和 p65 核转位以及 NF-B 驱动基因表达的诱导。我们证明 TWEAK 对 IL-8 表达的诱导可以被 LiCl 抵消。综上所述，这些数据表明 GSK-3beta 在 TWEAK 和 NF-B 之间的信号转导途径中发挥重要作用。 (C) 2004 年欧洲生化学会联合会。由 Elsevier B.V. 出版。保留所有权利。
Glycogen synthase kinase-3beta (GSK-3beta) is a key component of several signaling pathways. We found that a short variant of 'TNF-like weak inducer of apoptosis' (shortTWEAK) formed a complex with GSK-3beta in a yeast two-hybrid system. We demonstrate that shortTWEAK and GSK-3beta colocalize in the nucleus of human neuroblastoma cells. We also show that TWEAK is internalized in different cell lines and that it translocates to the nucleus. This event causes the degradation of IBalpha, the nuclear translocation of both GSK-3beta and p65, and the induction of NF-B-driven gene expression. We demonstrate that the induction of IL-8 expression by TWEAK can be counteracted by LiCl. Taken together, these data suggest that GSK-3beta plays an important role in the signal transduction pathway between TWEAK and NF-B. (C) 2004 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.