Arkinstall S, Emergy I, Church D, Chollet A, Kawashima E
Department of Biological Chemistry, Glaxo Institute for Molecular Biology, Geneva, Switzerland.
FEBS Lett. 1994 Jan 24;338(1):75-80. doi: 10.1016/0014-5793(94)80119-3.
We have cloned a cDNA encoding the human ileal neurokinin-2 (NK-2) receptor which mediates powerful neurokinin A-stimulated arachidonic acid (AA) and prostaglandin release when expressed in CHO cells. Two major signal transduction events appear to underlie this response. Firstly, AA liberation is critically dependent upon agonist-stimulated influx of extracellular Ca2+ although not release from intracellular stores. Secondly, NK-2 receptor-linked AA mobilization requires concomitant PKC activation and based upon limited subtype immunodetectability as well as toxin, identical pretreatment inhibits AA release partially and blocks PKC alpha translocation completely. These observations indicate that in this cell system AA liberation reflects NK-2 receptor-dependent activation of two distinct but converging signal transduction pathways regulated by different G-protein species and involving Ca2+ influx and PKC alpha activation.
我们克隆了一个编码人回肠神经激肽-2（NK-2）受体的cDNA，该受体在CHO细胞中表达时，可介导强大的神经激肽A刺激的花生四烯酸（AA）和前列腺素释放。两个主要的信号转导事件似乎是这种反应的基础。首先，AA的释放关键取决于激动剂刺激的细胞外Ca2+内流，而不是细胞内储存的释放。其次，NK-2受体相关的AA动员需要PKC的同时激活，基于有限的亚型免疫检测以及毒素，相同的预处理可部分抑制AA释放并完全阻断PKCα易位。这些观察结果表明，在这个细胞系统中，AA的释放反映了由不同G蛋白种类调节的两条不同但汇聚的信号转导途径的NK-2受体依赖性激活，涉及Ca2+内流和PKCα激活。
