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首页> 外文期刊>Cytokine >A functional role for interleukin (IL)-4-driven cyclic amp accumulation in human b lymphocytes.
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A functional role for interleukin (IL)-4-driven cyclic amp accumulation in human b lymphocytes.

机译:白细胞介素(IL)-4驱动的人耳b淋巴细胞中的循环安培积累的功能作用。

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摘要

Interleukin-4 (IL-4) regulates the expression of the 55-kDa alpha-subunit (CD25) of the IL-2 receptor complex in human B lymphocytes. This report suggests that the cAMP/protein kinase A (PKA) component of the IL-4 receptor signalling programme in human tonsillar B cells has a functionally important role in regulating expression of the CD25 gene by attenuating activity of a protein binding to a potent negative regulatory element (NRE) in the CD25 promoter; this effect can be mimicked by agents that elevate cAMP and blocked by inhibitors of PKA but not protein kinase C (PKC). In a B-cell line that fails to elevate cAMP, attenuate NRE-binding protein (NRE-BP) activity or express CD25 following IL-4 treatment, stimulation of cAMP accumulation by forskolin facilitates IL-4-mediated induction of both the endogenous gene and an exogenous reporter gene under the control of a minimal promoter/enhancer fragment of the CD25 gene. Copyright 2000 Academic Press.
机译:白介素-4(IL-4)调节人B淋巴细胞中IL-2受体复合物的55 kDaα-亚基(CD25)的表达。该报告表明,人扁桃体B细胞中IL-4受体信号传导程序中的cAMP /蛋白激酶A(PKA)成分在功能上起重要作用,可通过减弱与强阴性抗体结合的蛋白的活性来调节CD25基因的表达。 CD25启动子中的调控元件(NRE);这种作用可以通过升高cAMP的药物来模仿,而可以通过PKA的抑制剂而不是蛋白激酶C(PKC)来阻止。在IL-4处理后无法升高cAMP,减弱NRE结合蛋白(NRE-BP)活性或表达CD25的B细胞系中,福司柯林刺激cAMP蓄积促进了IL-4介导的两个内源基因的诱导在CD25基因的最小启动子/增强子片段的控制下的外源报道基因。版权所有2000学术出版社。

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