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首页> 外文期刊>Cellular Signalling >Differential regulation of p65 and c-Rel NF-kappa B transactivating activity by Cot, protein kinase C zeta and NIK protein kinases in CD3/CD28 activated T cells
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Differential regulation of p65 and c-Rel NF-kappa B transactivating activity by Cot, protein kinase C zeta and NIK protein kinases in CD3/CD28 activated T cells

机译：CD3 / CD28激活的T细胞中Cot，蛋白激酶C zeta和NIK蛋白激酶对p65和c-RelNF-κB反式激活活性的差异调节

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摘要

It has been shown that phosphorylation of p65/RelA and c-Rel plays a role in the regulation of transcriptional activity of NF-kappa B independent on I kappa B degradation. In this study, we show that anti CD3/CD28 activation induces the transactivation activity of both p65/RelA and c-Rel in T cells using Gal4 dependent assays. Moreover, protein kinase C (PKC)zeta, Cot kinase and NF-kappa B-inducing kinase (NIK) seem to be involved in those processes in a different manner. Thus, transfection of dominant negative forms of Cot and PKC inhibits CD3/CD28 induction of Gal4-p65 transactivation, whereas the kinase inactive versions of the 3 kinases inhibit induction of Gal4-c-Rel. Cot induction of Gal4-c-Rel transactivating activity seems to be mediated sequentially through PKC zeta and NIK activation, since dominant negative form of NIK blocks Cot and PKC zeta induction, whereas kinase inactive PKC zeta only blocks Cot activity. In contrast, the contribution of NIK to the transactivation function of p65/RelA seems to be negligible and more importantly NIK-KD did not inhibit induction by Cot and PKC zeta. Besides, the enhancing effect of Cot on Gal4-p65 was not decreased in mouse embryo fibroblasts from NIK deficient aly/aly mice in contrast with a greatest reduction on Gal4-c-Rel. By using Ser to Ala mutants in p65 and c-Rel transactivation domains, PKC zeta and NIK activities seem to be dependent of a restricted set of Ser in both proteins. In contrast, the enhancing effect of Cot seems to be less dependent of a particular set of Ser residues being partially abrogated by mutation of several Ser residues. (c) 2006 Elsevier Inc. All rights reserved.
机译：已经显示p65 / RelA和c-Rel的磷酸化在独立于IκB降解的NF-κB转录活性的调节中起作用。在这项研究中，我们显示抗CD3 / CD28激活使用Gal4依赖性测定诱导T细胞中p65 / RelA和c-Rel的反式激活活性。此外，蛋白激酶C（PKC）zeta，Cot激酶和NF-κB诱导激酶（NIK）似乎以不同的方式参与了这些过程。因此，转染Cot和PKC的负性显性负型抑制了Gal4-p65反式激活的CD3 / CD28诱导，而3种激酶的激酶非活性形式抑制了Gal4-c-Rel的诱导。 Gal4-c-Rel反式激活活性的婴儿床诱导似乎是通过PKC zeta和NIK活化顺序介导的，因为NIK的显性负性形式会阻断Cot和PKC zeta诱导，而激酶失活的PKC zeta仅阻断Cot活性。相反，NIK对p65 / RelA反式激活功能的贡献似乎可以忽略不计，更重要的是NIK-KD不会抑制Cot和PKC zeta的诱导。另外，与来自Gal4-c-Rel的最大降低相反，来自NIK缺陷的aly / aly小鼠的小鼠胚胎成纤维细胞中Cot对Gal4-p65的增强作用并未降低。通过在p65和c-Rel反式激活域中使用Ser到Ala突变，PKC zeta和NIK活性似乎取决于这两种蛋白中Ser的受限集。相比之下，Cot的增强作用似乎较少依赖于特定的Ser残基组，该残基通过几个Ser残基的突变而被部分废除。 （c）2006 Elsevier Inc.保留所有权利。

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