Grassie M A, Milligan G
Molecular Pharmacology Group, University of Glasgow, Scotland, U.K.
Biochem J. 1995 Mar 1;306 ( Pt 2)(Pt 2):525-30. doi: 10.1042/bj3060525.
Rat 1 fibroblasts which had been transfected to express the human alpha 2C10 adrenoceptor (clone 1C) were further co-transfected with a plasmid containing the hygromycin-B-resistance gene and a plasmid containing a cDNA encoding the alpha-subunit of the rat pertussis-toxin-sensitive G-protein G(o)1. In clone 3 the receptor was expressed at some 2.2 pmol/mg of membrane protein, and G(o)1 alpha at approx. 100 pmol/mg of membrane protein. The interaction of these two polypeptides and that between the receptor and Gi2 alpha (endogenously expressed at some 50 pmol/mg of membrane protein) were studied. Agonist activation of G(o)1 alpha was observed in membranes of the alpha 2C10-adrenoceptor(+)-G(o)1 alpha+ cells (clone 3), but not in alpha 2C10-adrenoceptor(+)-G(o)alpha-cells (clone 1C), whereas similar agonist-dependent activation of Gi2 alpha was observed in both cell types. alpha 2C10-adrenoceptor activation of G(o)1 alpha and Gi2 alpha in clone-3 membranes was produced with similar agonist-dose-effect curves. These observations indicate that the receptor interacts with equivalent affinity with each of these G-proteins. Agonist-dependent cholera-toxin-catalysed [32P]ADP-ribosylation of G(o)1 alpha was terminated when the alpha 2-adrenoceptor antagonist yohimbine was added subsequent to agonist-induced initiation of the reaction and release of GDP, demonstrating the conformational requirement for this reaction to be the ternary complex of agonist-occupied receptor and guanine-nucleotide-denuded G-protein.
已转染以表达人α2C10肾上腺素能受体(克隆1C)的大鼠1成纤维细胞,进一步与含有潮霉素B抗性基因的质粒和含有编码大鼠百日咳毒素敏感G蛋白G(o)1α亚基的cDNA的质粒共转染。在克隆3中,受体以约2.2 pmol/mg膜蛋白的水平表达,G(o)1α约为100 pmol/mg膜蛋白。研究了这两种多肽之间的相互作用以及受体与Gi2α(内源性表达水平约为50 pmol/mg膜蛋白)之间的相互作用。在α2C10 - 肾上腺素能受体(+) - G(o)1α +细胞(克隆3)的膜中观察到激动剂对G(o)1α的激活,但在α2C10 - 肾上腺素能受体(+) - G(o)α -细胞(克隆1C)中未观察到,而在两种细胞类型中均观察到类似的激动剂依赖性Gi2α激活。克隆3膜中α2C10 - 肾上腺素能受体对G(o)1α和Gi2α的激活具有相似的激动剂剂量 - 效应曲线。这些观察结果表明,受体与这些G蛋白中的每一种以等效亲和力相互作用。当在激动剂诱导反应起始并释放GDP后加入α2 - 肾上腺素能受体拮抗剂育亨宾时,激动剂依赖性霍乱毒素催化的G(o)1α的[32P] ADP - 核糖基化终止,证明该反应的构象要求是激动剂占据的受体和鸟嘌呤核苷酸去除的G蛋白的三元复合物。