Johnson M L, Ackers G K
Biochemistry. 1982 Jan 19;21(2):201-11. doi: 10.1021/bi00531a001.
The stereochemical postulates of Perutz for the mechanism of hemoglobin [Perutz, M. F. (1970) Nature (London) 228, 726--739] have been formulated into a statistical thermodynamic model. The model is based on that of Szabo and Karplus [Szabo, A., & Karplus, M. (1972) J. Mol. Biol 72, 163--197] but has been extended to include the properties of dissociated dimers in equilibrium with tetramers. The dissociation eliminates the alpha 1 beta 2 intersubunit contact which is the major site of ligand-linked structure change. The model quantitatively describes the coupling between binding of oxygen and protons in dimers and tetramers, the change in quaternary structure, and the breaking of salt bridges which are assumed to stabilize the deoxy quaternary structure. The extended model has been tested against an extensive series of recent experimental data from our laboratory and elsewhere on the ligand-linked dimer-tetramer assembly in normal human hemoglobin A and in the variant hemoglobin Kansas (beta 102 Asp leads to Asn). Two versions of the model were used which differ in the properties of the dissociated dimers. For both hemoglobins, the models were found capable of simultaneously describing the data on the ligand-linked dimer-tetramer assembly and predicting the tetramer Bohr effect. However, neither model predicted reasonable values for the tetramer Bohr effect without simultaneously predicting unreasonable values for the affinities of individual chains. Both models incorrectly predict preferential binding of oxygen to the alpha or beta chains within the tetramer. These results argue against the Perutz mechanism for the molecular processes of hemoglobin.
佩鲁茨提出的关于血红蛋白作用机制的立体化学假设[佩鲁茨,M. F.(1970年)《自然》(伦敦)228, 726 - 739]已被转化为一个统计热力学模型。该模型基于萨博和卡尔普斯的模型[萨博,A.,&卡尔普斯,M.(1972年)《分子生物学杂志》72, 163 - 197],但已扩展到包括与四聚体处于平衡状态的解离二聚体的性质。解离消除了α1β2亚基间接触,而该接触是配体连接的结构变化的主要位点。该模型定量描述了二聚体和四聚体中氧和质子结合之间的耦合、四级结构的变化以及假定稳定脱氧四级结构的盐桥的断裂。针对我们实验室及其他地方最近关于正常人血红蛋白A和变异血红蛋白堪萨斯(β102天冬氨酸突变为天冬酰胺)中配体连接的二聚体 - 四聚体组装的一系列广泛实验数据,对扩展模型进行了检验。使用了该模型的两个版本,它们在解离二聚体的性质方面有所不同。对于这两种血红蛋白,发现模型能够同时描述配体连接的二聚体 - 四聚体组装的数据并预测四聚体玻尔效应。然而,没有一个模型在不同时预测单个链亲和力的不合理值的情况下,能预测出合理的四聚体玻尔效应值。两个模型都错误地预测了氧在四聚体内优先与α链或β链结合。这些结果对血红蛋白分子过程的佩鲁茨机制提出了质疑。