Tsai S C, Noda M, Adamik R, Chang P P, Chen H C, Moss J, Vaughan M
Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892.
J Biol Chem. 1988 Feb 5;263(4):1768-72.
Choleragen (cholera toxin) activates adenylate cyclase by catalyzing ADP-ribosylation of Gs alpha, the stimulatory guanine nucleotide-binding protein. It was recently found (Tsai, S.-C., Noda, M., Adamik, R., Moss, J., and Vaughan, M. (1987) Proc. Natl. Acad. Sci. U. S. A. 84, 5139-5142) that a bovine brain membrane protein known as ADP-ribosylation factor or ARF, which enhances ADP-ribosylation of Gs alpha, also increases the GTP-dependent NAD:arginine and NAD:protein ADP-ribosyltransferase, NAD glycohydrolase, and auto-ADP-ribosylation activities of choleragen. We report here the purification and characterization of two soluble proteins from bovine brain that similarly enhance the Gs alpha-dependent and independent ADP-ribose transfer reactions catalyzed by toxin. Like membrane ARF, both soluble factors are 19-kDA proteins dependent on GTP or GTP analogues for activity. Maximal ARF effects were observed at a molar ratio of less than 2:1, ARF/toxin A subunit. Dimyristoyl phosphatidylcholine was necessary for optimal ADP-ribosylation of Gs alpha but inhibited auto-ADP-ribosylation of the choleragen A1 subunit and NAD:agmatine ADP-ribosyltransferase activity. It appears that the soluble factors directly activate choleragen in a GTP-dependent fashion. The relationships of the ARF proteins to the ras oncogene products and to the family of guanine nucleotide-binding regulatory proteins that includes Gs alpha remains to be determined.
霍乱毒素通过催化刺激性鸟嘌呤核苷酸结合蛋白Gsα的ADP核糖基化来激活腺苷酸环化酶。最近发现(蔡,S.-C.,野田,M.,阿达米克,R.,莫斯,J.,和沃恩,M.(1987年)美国国家科学院院刊84,5139 - 5142),一种被称为ADP核糖基化因子或ARF的牛脑膜蛋白,它增强Gsα的ADP核糖基化,也增加霍乱毒素的GTP依赖性NAD:精氨酸和NAD:蛋白质ADP核糖基转移酶、NAD糖水解酶以及自身ADP核糖基化活性。我们在此报告从牛脑中纯化和鉴定的两种可溶性蛋白,它们同样增强毒素催化的Gsα依赖性和非依赖性ADP核糖转移反应。与膜ARF一样,这两种可溶性因子都是19-kDA蛋白,其活性依赖于GTP或GTP类似物。在ARF/毒素A亚基的摩尔比小于2:1时观察到最大的ARF效应。二肉豆蔻酰磷脂酰胆碱对于Gsα的最佳ADP核糖基化是必需的,但抑制霍乱毒素A1亚基的自身ADP核糖基化和NAD:胍丁胺ADP核糖基转移酶活性。看来这些可溶性因子以GTP依赖性方式直接激活霍乱毒素。ARF蛋白与ras癌基因产物以及包括Gsα在内的鸟嘌呤核苷酸结合调节蛋白家族之间的关系仍有待确定。