Marciniszyn J, Huang J S, Hartsuck J A, Tang J
J Biol Chem. 1976 Nov 25;251(22):7095-102.
Intramolecular pepsinogen activation is inhibited either by pepstatin, a potent pepsin inhibitor, or by purified globin from hemoglobin, a good pepsin substrate. Also, pepsinogen at pH 2 can be bound to a pepstatin-Sepharose column and recovered as native zymogen upon elution in pH 8 buffer. Kinetic studies of the globin inhibition of pepsinogen activation show that globin binds to a pepsinogen intermediate. This interaction gives rise to competitive inhibition of intramolecular pepsinogen activation. The evidence presented in this paper suggests that pepsinogen is converted rapidly upon acidification to the pepsinogen intermediate delta. In the absence of an inhibitor, the intermediate undergoes conformational change to bind the activation peptide portion of this same pepsinogen molecule in the active center to form an intramolecular enzyme-substrate complex (intermediate theta). This is followed by the intramolecular hydrolysis of the peptide bond between residues 44 and 45 of the pepsinogen molecule and the dissociation of the activation peptide from the pepsin. Intermediate delta apparently does not activate another pepsinogen molecule via an intermolecular process. Neither does intermediate delta hydrolyze globin substrate.
分子内胃蛋白酶原激活可被强力胃蛋白酶抑制剂胃抑素或血红蛋白中的纯化珠蛋白(一种良好的胃蛋白酶底物)抑制。此外,pH 2条件下的胃蛋白酶原可与胃抑素 - 琼脂糖柱结合,并在pH 8缓冲液洗脱时作为天然酶原回收。珠蛋白对胃蛋白酶原激活的抑制动力学研究表明,珠蛋白与胃蛋白酶原中间体结合。这种相互作用导致分子内胃蛋白酶原激活的竞争性抑制。本文提供的证据表明,胃蛋白酶原在酸化后迅速转化为胃蛋白酶原中间体δ。在没有抑制剂的情况下,中间体发生构象变化,以结合活性中心中同一胃蛋白酶原分子的激活肽部分,形成分子内酶 - 底物复合物(中间体θ)。随后,胃蛋白酶原分子第44和45位残基之间的肽键发生分子内水解,激活肽从胃蛋白酶上解离。中间体δ显然不会通过分子间过程激活另一个胃蛋白酶原分子。中间体δ也不会水解珠蛋白底物。