Diacylglycerol kinase α enhances protein kinase Cζ-dependent phosphorylation at Ser311 of p65/RelA subunit of nuclear factor-κB
Diacylglycerol kinase α enhances protein kinase Cζ-dependent phosphorylation at Ser311 of p65/RelA subunit of nuclear factor-κB
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DOI：
10.1016/j.febslet.2009.09.017
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发表时间：
2009-10-06
期刊：
影响因子：
3.5
通讯作者：
Sakane, Fumio
中科院分区：
文献类型：
--
作者：
Kai, Masahiro;Yasuda, Satoshi;Sakane, Fumio
我们最近报道，二酰甘油激酶（DGK）α增强肿瘤坏死因子-α（TNF-α）诱导的核因子-κ B（NF-κ B）活化。然而，DGK α和NF-κ B B之间的信号传导通路仍不清楚。在此，我们发现小干扰RNA介导的DGK α敲低强烈减弱NF-κ B B大亚基p65/RelA在Ser 311的蛋白激酶C（PKC）zeta依赖性磷酸化，但不减弱PKC zeta非依赖性Ser 468或Ser 536磷酸化。此外，PKC zeta的敲低和过表达分别抑制和协同增强DGK α介导的NF-κ B活化。这些结果强烈表明DGKa通过PKC zeta介导的p65/RelA的Ser 311磷酸化正调节TNF-α依赖的NF-κ B活化。(C)2009年欧洲生物化学学会联合会。Elsevier B. V.出版，保留所有权利。
We recently reported that diacylglycerol kinase (DGK) alpha enhanced tumor necrosis factor-alpha (TNF-alpha)-induced activation of nuclear factor-kappa B (NF-kappa B). However, the signaling pathway between DGK alpha and NF-kappa B remains unclear. Here, we found that small interfering RNA-mediated knockdown of DGK alpha strongly attenuated protein kinase C (PKC) zeta-dependent phosphorylation of a large subunit of NF-kappa B, p65/RelA, at Ser311 but not PKC zeta-independent phosphorylation at Ser468 or Ser536. Moreover, knockdown and overexpression of PKC zeta suppressed and synergistically enhanced DGK alpha-mediated NF-kappa B activation, respectively. These results strongly suggest that DGKa positively regulates TNF-alpha-dependent NF-kappa B activation via the PKC zeta-mediated Ser311 phosphorylation of p65/RelA. (C) 2009 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.