百日咳毒素介导的兔黄体Gi的ADP核糖基化作用使脑啡肽对腺苷酸环化酶的抑制作用解偶联。

Some of the actions of pertussis toxin on the rabbit luteal adenylyl cyclase system were analyzed. 2. Incubation of luteal membranes with pertussis toxin and [32P]NAD resulted in the [32P]ADP-ribosylation of a 40,000 Da protein that is distinct from the proteins ADP-ribosylated by cholera toxin. 3. Pertussis toxin specific [32P]ADP-ribosylation was time-dependent and dependent upon the concentration of pertussis toxin present during the incubation. 4. Pertussis toxin mediated [32P]ADP-ribosylation was enhanced by ATP, ADP, adenylyl imidodiphosphate, GTP, guanosine-5'-O-(2-thiodiphosphate), guanosine-5'-O-(3-thiotriphosphate), and NaF but not AMP or guanylyl imidodiphosphate [GMP-P(NH)P]. 5. Treatment of luteal membranes with NAD and pertussis toxin prevents GTP and enkephalin but not GMP-P(NH)P mediated inhibition of forskolin stimulated adenylyl cyclase, demonstrating the existence of a functional Gi in the rabbit corpus luteum.

分析了百日咳毒素对兔黄体腺苷酸环化酶系统的一些作用。2. 用百日咳毒素和[32P]NAD孵育黄体膜，导致一种40,000 Da蛋白质的[32P]ADP核糖基化，该蛋白质不同于被霍乱毒素ADP核糖基化的蛋白质。3. 百日咳毒素特异性[32P]ADP核糖基化是时间依赖性的，并且取决于孵育期间存在的百日咳毒素浓度。4. ATP、ADP、腺苷酰亚胺二磷酸、GTP、鸟苷-5'-O-(2-硫代二磷酸)、鸟苷-5'-O-(3-硫代三磷酸)和NaF可增强百日咳毒素介导的[32P]ADP核糖基化，但AMP或鸟苷酰亚胺二磷酸[GMP-P(NH)P]则不能。5. 用NAD和百日咳毒素处理黄体膜可防止GTP和脑啡肽介导的对福斯可林刺激的腺苷酸环化酶的抑制，但不能防止GMP-P(NH)P介导的抑制，这表明兔黄体中存在功能性Gi。

Pertussis toxin-mediated ADP-ribosylation of rabbit luteal Gi uncouples enkephalin inhibition of adenylyl cyclase.