Wüster M, Costa T, Aktories K, Jakobs K H
Biochem Biophys Res Commun. 1984 Sep 28;123(3):1107-15. doi: 10.1016/s0006-291x(84)80247-8.
Pretreatment of intact NG108-15 cells with pertussis toxin suppresses opioid inhibition of cyclic AMP accumulation mediated by the inhibitory guanine nucleotide-binding regulatory protein, Ni, which apparently also mediates the inhibitory nucleotide effects on opioid against binding. The toxin treatment had no effect on opioid agonist binding measured in NG108-15 cell membranes without sodium present. However, the toxin potentiated the inhibitory effect of sodium on agonist binding, leading to an agonist-specific reduction of opioid receptor affinity in the presence of sodium in the binding reaction. The potency of the stable GTP analog, GTP gamma S, to reduce agonist binding in the presence of sodium was little changed in membranes prepared from pertussis toxin-treated cells compared to control membranes, whereas the potency of the stable GDP analog, GDP beta S, was magnified. The data indicate that ADP-ribosylation of Ni by pertussis toxin potentiates sodium regulation of opioid agonist binding and that the communication between Ni and opioid receptors is not lost by the covalent modification of Ni.
用百日咳毒素预处理完整的NG108 - 15细胞，可抑制阿片类物质对由抑制性鸟嘌呤核苷酸结合调节蛋白Ni介导的环磷酸腺苷积累的抑制作用，该蛋白显然也介导了抑制性核苷酸对阿片类物质结合的影响。毒素处理对在无钠存在的NG108 - 15细胞膜中测得的阿片类激动剂结合没有影响。然而，毒素增强了钠对激动剂结合的抑制作用，导致在结合反应中有钠存在时阿片受体亲和力出现激动剂特异性降低。与对照膜相比，在由百日咳毒素处理的细胞制备的膜中，稳定的GTP类似物GTPγS在有钠存在时降低激动剂结合的效力变化不大，而稳定的GDP类似物GDPβS的效力则增强。数据表明，百日咳毒素对Ni的ADP核糖基化增强了钠对阿片类激动剂结合的调节作用，并且Ni与阿片受体之间的通讯不会因Ni的共价修饰而丧失。
