首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Intracellular signaling of tumor necrosis factor-alpha in brain microvascular endothelial cells is mediated by a protein tyrosine kinase and protein kinase C-dependent pathway.
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Intracellular signaling of tumor necrosis factor-alpha in brain microvascular endothelial cells is mediated by a protein tyrosine kinase and protein kinase C-dependent pathway.

机译:脑微血管内皮细胞中肿瘤坏死因子-α的细胞内信号传导是由蛋白酪氨酸激酶和蛋白激酶C依赖性途径介导的。

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摘要

The intracellular signaling pathways responsible for tumor necrosis factor (TNF)-alpha stimulation of lymphocyte adhesion to brain microvascular endothelial cells (BMEC) were studied using inhibitors of protein kinase C (bisindolylmaleimide HCl, H-7, or staurosporine), or protein tyrosine kinase (genistein). Each of these blocked the ability of BMEC to respond to TNF-alpha. In contrast, BMEC treated with H-89, an inhibitor of protein kinase A, or the adenylate cyclase inhibitor, dideoxyadenosine, responded normally to TNF-alpha. Forskolin, an adenylate cyclase agonist, significantly increased lymphocyte adhesion to BMEC. These data indicate that intracellular signaling by TNF-alpha in BMEC is mediated through a protein kinase C and tyrosine kinase dependent pathway.
机译:使用蛋白激酶C(bisindolylmaleimide HCl,H-7或staurosporine)或蛋白酪氨酸激酶的抑制剂研究了负责肿瘤坏死因子(TNF)-α刺激淋巴细胞粘附至脑微血管内皮细胞(BMEC)的细胞内信号传导途径(染料木黄酮)。这些中的每一个都阻断了BMEC对TNF-α反应的能力。相反,用蛋白激酶A抑制剂H-89或腺​​苷酸环化酶抑制剂双脱氧腺苷H-89处理的BMEC对TNF-α正常反应。 Forskolin是一种腺苷酸环化酶激动剂,可显着增加淋巴细胞对BMEC的粘附力。这些数据表明BMEC中TNF-α的细胞内信号传导是通过蛋白激酶C和酪氨酸激酶依赖性途径介导的。

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