Veine D M, Ohnishi K, Williams C H
Department of Veterans Affairs Medical Center, Ann Arbor, Michigan 48105, USA.
Protein Sci. 1998 Feb;7(2):369-75. doi: 10.1002/pro.5560070217.
Thioredoxin reductase is a flavoprotein which catalyzes the reduction of the small protein thioredoxin by NADPH. It contains a redox active disulfide and an FAD in each subunit of its dimeric structure. Each subunit is further divided into two domains, the FAD and the pyridine nucleotide binding domains. The orientation of the two domains determined from the crystal structure and the flow of electrons determined from mechanistic studies suggest that thioredoxin reductase requires a large conformational change to carry out catalysis (Williams CH Jr, 1995, FASEB J 9:1267-1276). The constituent amino acids of an ion pair, E48/R130, between the FAD and pyridine nucleotide binding domains, were mutagenized to cysteines to form E48C,R130C (CC mutant). Formation of a stable bridge between these cysteines was expected to restrict the enzyme largely in the conformation observed in the crystal structure. Crosslinking with the bifunctional reagent N,N,1,2 phenylenedimaleimide, spanning 4-9 A, resulted in a >95 % decrease in thioredoxin reductase and transhydrogenase activity. SDS-PAGE confirmed that the crosslink in the CC-mutant was intramolecular. Dithionite titration showed an uptake of electrons as in wild-type enzyme, but anaerobic reduction of the flavin with NADPH was found to be impaired. This indicates that the crosslinked enzyme is in the conformation where the flavin and the active site disulfide are in close proximity but the flavin and pyridinium rings are too far apart for effective electron transfer. The evidence is consistent with the hypothesis that thioredoxin reductase requires a conformational change to complete catalysis.
硫氧还蛋白还原酶是一种黄素蛋白,它催化由NADPH还原小蛋白硫氧还蛋白。在其二聚体结构的每个亚基中,它含有一个氧化还原活性二硫键和一个FAD。每个亚基进一步分为两个结构域,即FAD和吡啶核苷酸结合结构域。根据晶体结构确定的两个结构域的方向以及根据机理研究确定的电子流动表明,硫氧还蛋白还原酶需要进行大的构象变化才能进行催化(小威廉姆斯·C·H,1995年,《美国实验生物学会联合会杂志》9:1267 - 1276)。FAD和吡啶核苷酸结合结构域之间离子对E48/R130的组成氨基酸被突变为半胱氨酸,形成E48C、R130C(CC突变体)。预计这些半胱氨酸之间形成稳定的桥会使酶在很大程度上限制于晶体结构中观察到的构象。用跨度为4 - 9埃的双功能试剂N,N,1,2 - 苯二马来酰亚胺进行交联,导致硫氧还蛋白还原酶和转氢酶活性降低>95%。SDS - PAGE证实CC突变体中的交联是分子内的。连二亚硫酸盐滴定显示与野生型酶一样有电子摄取,但发现用NADPH对黄素进行厌氧还原受到损害。这表明交联后的酶处于黄素与活性位点二硫键紧密相邻,但黄素与吡啶环相距太远而无法进行有效电子转移的构象。该证据与硫氧还蛋白还原酶需要构象变化来完成催化的假设一致。