Bruni P, Hewlett E L, Moss J
Biochem Biophys Res Commun. 1985 Mar 29;127(3):999-1006. doi: 10.1016/s0006-291x(85)80043-7.
Release of bound [3H]Gpp(NH)p from NG108-15 cell membranes was induced by carbamylcholine, enkephalinamide, and norepinephrine, all of which inhibit adenylate cyclase. Release was blocked by antagonist, was greater with multiple agonists than with one, and required guanyl nucleotides. With membranes from pertussis toxin-treated cells, both total [3H] Gpp(NH)p binding and agonist-induced [3H]Gpp(NH)p release was decreased. ADP-ribosylation by toxin of transducin, the retinal GTP-binding protein which is similar in structure and function to that in cyclase, decreased [3H]Gpp(NH)p binding. Thus, the inability to demonstrate agonist-induced [3H]Gpp(NH)p release from toxin-treated NG108-15 membranes may result in part from absence of bound [3H]Gpp(NH)p.
氨甲酰胆碱、脑啡肽酰胺和去甲肾上腺素可诱导NG108 - 15细胞膜中结合的[³H]Gpp(NH)p释放,这些物质均抑制腺苷酸环化酶。拮抗剂可阻断释放,多种激动剂诱导的释放比单一激动剂诱导的释放更大,且需要鸟苷核苷酸。对于百日咳毒素处理过的细胞的膜,总的[³H]Gpp(NH)p结合以及激动剂诱导的[³H]Gpp(NH)p释放均减少。转导蛋白是视网膜GTP结合蛋白,其结构和功能与环化酶中的相似,毒素对转导蛋白进行的ADP - 核糖基化作用降低了[³H]Gpp(NH)p结合。因此,无法证明毒素处理过的NG108 - 15细胞膜存在激动剂诱导的[³H]Gpp(NH)p释放,这可能部分是由于缺乏结合的[³H]Gpp(NH)p所致。