Pettit F H, Humphreys J, Reed L J
Proc Natl Acad Sci U S A. 1982 Jul;79(13):3945-8. doi: 10.1073/pnas.79.13.3945.
Endogenous kinase activity of highly purified pyruvate dehydrogenase complex from bovine kidney is markedly inhibited by N-ethylmaleimide and by certain disulfides. Inhibition by disulfides is highly specific and is reversed by thiols. 5,5'-Dithiobis(2-nitrobenzoate) is the most potent inhibitor, showing significant inhibition at a concentration as low as 1 microM. Cystamine, oxidized glutathione, pantethine, lipoic acid, lipoamide, ergothionine, insulin, oxytocin, and vasopressin were ineffective. Hydrogen peroxide and t-butyl hydroperoxide were inactive. The data indicate pyruvate dehydrogenase kinase (EC 2.7.1.99) contains a thiol group (or groups) that is involved in maintaining a conformation of the enzyme that facilitates phosphorylation and inactivation of its protein substrate, pyruvate dehydrogenase (EC 1.2.4.1). These findings suggest that modulation of pyruvate dehydrogenase kinase activity by thiol-disulfide exchange may be an important physiological mechanism for regulation of kinase activity and, hence, activity of the pyruvate dehydrogenase complex.
牛肾中高度纯化的丙酮酸脱氢酶复合体的内源性激酶活性受到N-乙基马来酰亚胺和某些二硫化物的显著抑制。二硫化物的抑制作用具有高度特异性,且可被硫醇逆转。5,5'-二硫代双(2-硝基苯甲酸)是最有效的抑制剂,在低至1微摩尔的浓度下就表现出显著抑制作用。胱胺、氧化型谷胱甘肽、泛硫乙胺、硫辛酸、硫辛酰胺、麦角硫因、胰岛素、催产素和加压素均无效。过氧化氢和叔丁基过氧化氢无活性。数据表明,丙酮酸脱氢酶激酶(EC 2.7.1.99)含有一个(或多个)硫醇基团,该基团参与维持酶的构象,从而促进其蛋白质底物丙酮酸脱氢酶(EC 1.2.4.1)的磷酸化和失活。这些发现表明,通过硫醇-二硫化物交换调节丙酮酸脱氢酶激酶活性可能是调节激酶活性以及丙酮酸脱氢酶复合体活性的重要生理机制。