首页> 外文期刊>Bulletin of experimental biology and medicine >BCL11B Upregulates the Expression of RelA in T Cells Stimulated with Staphylococcal Enterotoxin A
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BCL11B Upregulates the Expression of RelA in T Cells Stimulated with Staphylococcal Enterotoxin A

机译:BCL11B 上调葡萄球菌肠毒素 A 刺激的 T 细胞中 RelA 的表达

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摘要

We explored the potential link between RelA and BCL11B transcription factors. To this end, Jurkat and Raji cells (Jurkat:Raji 10:1), as well as normal human peripheral blood T cells, were activated by staphylococcal enterotoxin A (SEA) and the expressions of both BCL11B and RelA mRNA and proteins were detected. BCL11B small interfering RNA was then transduced into Jurkat cells. Under the effect of SEA stimulation, the expression of BCL11B and RelA mRNA increased in two types of T cell lines over time, and the results were comparable with the levels of expression of BCL11B and RelA proteins. In the BCL11B-knockdown cells, the expression of RelA protein did not increase. These findings suggest that BCL11B regulates RelA expression in Jurkat cells and human peripheral blood T cells from healthy donors via the T-cell receptor signaling pathway.
机译:我们探索了 RelA 和 BCL11B 转录因子之间的潜在联系。为此,葡萄球菌肠毒素 A (SEA) 激活了 Jurkat 和 Raji 细胞 (Jurkat:Raji 10:1) 以及正常人外周血 T 细胞,并检测了 BCL11B 和 RelA mRNA 和蛋白质的表达。然后将BCL11B小干扰RNA转导到Jurkat细胞中。在SEA刺激作用下,两种T细胞系中BCL11B和RelA mRNA的表达随时间增加,结果与BCL11B和RelA蛋白的表达水平相当。在BCL11B敲低细胞中,RelA蛋白的表达没有增加。这些发现表明,BCL11B 通过 T 细胞受体信号通路调节来自健康供体的 Jurkat 细胞和人外周血 T 细胞中 RelA 的表达。

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