Moss J, Vaughan M
Proc Natl Acad Sci U S A. 1978 Aug;75(8):3621-4. doi: 10.1073/pnas.75.8.3621.
An ADP-ribosyltransferase was purified approximately 500-fold from the supernatant fraction of turkey erythrocytes. The enzyme hydrolyzed [carbonyl-(14)C]NAD to ADP-ribose and [carbonyl-(14)C]nicotinamide at a low rate. Nicotinamide formation from NAD was enhanced by arginine methyl ester > D-arginine approximately L-arginine > guanidine; lysine, histidine, and citrulline were ineffective. Incubation of [adenine-U-(14)C]NAD and arginine methyl ester or arginine with the purified enzyme resulted in the formation of new compounds that contained (14)C, reacted with ninhydrin, and quenched background fluorescence of thin-layer plates viewed in ultraviolet light. Their mobilities on thin-layer chromatograms were indistinguishable from those of ADP-ribosylarginine methyl ester and ADP-ribosylarginine formed during incubation of choleragen with NAD and arginine methyl ester or arginine, respectively [Moss, J. & Vaughan, M. (1977) J. Biol. Chem. 252, 2455-2457]. The purified transferase also catalyzed the incorporation of label from [adenine-(14)C]-NAD into lysozyme, histones and polyarginine. When the (14)C-labeled lysozyme was incubated with snake venom phosphodiesterase, the radioactivity was released and, on thin-layer chromatograms, exhibited a mobility indistinguishable from that of 5'-AMP, as would be expected of an ADP-ribosylated protein, but not of a poly(ADP-ribosylated) product. The purified transferase activated rat brain adenylate cyclase and, as is the case with choleragen, activation was absolutely dependent on NAD. The presence in the avian erythrocyte of a protein that, like choleragen and Escherichia coli heat-labile enterotoxin, apparently activates adenylate cyclase and possesses ADP-ribosyl transferase activity is consistent with the view that the mechanisms through which the bacterial toxins produce pathology are not entirely foreign to vertebrate cells, at least some of which may possess and employ an analogous mechanism for activation of adenylate cyclase.
从火鸡红细胞的上清液组分中纯化出一种ADP - 核糖基转移酶,纯化倍数约为500倍。该酶以低速率将[羰基 - (14)C]NAD水解为ADP - 核糖和[羰基 - (14)C]烟酰胺。精氨酸甲酯>D - 精氨酸>L - 精氨酸>胍可增强由NAD形成烟酰胺的反应;赖氨酸、组氨酸和瓜氨酸则无作用。将[腺嘌呤 - U - (14)C]NAD与精氨酸甲酯或精氨酸与纯化的酶一起温育,会形成含有(14)C的新化合物,这些化合物与茚三酮反应,并淬灭在紫外线下观察的薄板背景荧光。它们在薄板色谱图上的迁移率与分别在霍乱毒素与NAD和精氨酸甲酯或精氨酸温育过程中形成的ADP - 核糖基精氨酸甲酯和ADP - 核糖基精氨酸的迁移率无法区分[莫斯,J. & 沃恩,M. (1977) J. 生物化学杂志. 252, 2455 - 2457]。纯化的转移酶还催化将[腺嘌呤 - (14)C] - NAD中的标记掺入溶菌酶、组蛋白和聚精氨酸中。当将(14)C标记的溶菌酶与蛇毒磷酸二酯酶一起温育时,放射性被释放,并且在薄板色谱图上显示出与5'-AMP无法区分的迁移率,这正如ADP - 核糖基化蛋白质所预期的那样,但不是聚(ADP - 核糖基化)产物的迁移率。纯化的转移酶激活大鼠脑腺苷酸环化酶,并且与霍乱毒素的情况一样,激活绝对依赖于NAD。禽类红细胞中存在一种蛋白质,它与霍乱毒素和大肠杆菌不耐热肠毒素一样,显然激活腺苷酸环化酶并具有ADP - 核糖基转移酶活性,这与细菌毒素产生病理的机制并非完全不同于脊椎动物细胞的观点一致,至少其中一些细胞可能拥有并采用类似的机制来激活腺苷酸环化酶。