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利用巨噬细胞一氧化氮合酶的分离加氧酶和还原酶结构域重建一氧化氮合成的第二步。

Reconstitution of the second step in NO synthesis using the isolated oxygenase and reductase domains of macrophage NO synthase.

作者信息

Ghosh D K, Abu-Soud H M, Stuehr D J

机构信息

Department of Immunology, Cleveland Clinic Research Institute, Ohio 44195, USA.

出版信息

Biochemistry. 1995 Sep 12;34(36):11316-20. doi: 10.1021/bi00036a003.

Abstract

Inducible macrophage NO synthase (iNOS) is a homodimer of 130 kDa subunits. Trypsinolysis of iNOS inactivates its NO synthesis activity and cleaves the enzyme into a dimeric oxygenase fragment that contains heme, tetrahydrobiopterin, and the substrate binding site and a monomeric reductase fragment that contains FAD, FMN, calmodulin, and the binding site for NADPH [Ghosh, D. I., & Stuehr, D. H. (1995) Biochemistry 34, 801-807]. In this paper, we describe the reconstitution of NO synthesis activity utilizing the isolated oxygenase and reductase domains of iNOS. Mixing the domains at various ratios showed that NO was not produced from L-arginine but could be formed from the reaction intermediate N omega-hydroxy-L-arginine (L-NOHA). The apparent Km with L-NOHA in the reconstituted system was 100 microM versus 19 microM for native iNOS. D-NOHA was not a substrate. Maximum specific activity (per heme) occurred at an oxygenase to reductase molar ratio of 4:1, with higher ratios causing some inhibition. Reconstitution of activity was associated with electron transfer between the domain fragments and led to an incomplete reduction of the oxygenase domain heme iron. L-NOHA, but not L-arginine, increased NADPH consumption in the reconstituted system. Between 2.5 and 3.0 NADPH were consumed per NO formed from L-NOHA, considerably higher than the stoichiometry obtained with native iNOS (0.5 NADPH oxidized per NO formed), indicating an uncoupled electron transfer between the domain fragments. Thus, the isolated iNOS reductase and oxygenase domains each retain their separate catalytic functions but interact to catalyze only the second step of NO synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

诱导型巨噬细胞一氧化氮合酶(iNOS)是由130 kDa亚基组成的同型二聚体。iNOS经胰蛋白酶消化后会使其一氧化氮合成活性丧失,并将该酶裂解为一个包含血红素、四氢生物蝶呤和底物结合位点的二聚体加氧酶片段以及一个包含黄素腺嘌呤二核苷酸(FAD)、黄素单核苷酸(FMN)、钙调蛋白和烟酰胺腺嘌呤二核苷酸磷酸(NADPH)结合位点的单体还原酶片段[戈什,D. I.,& 斯图尔,D. H.(1995年)《生物化学》34卷,801 - 807页]。在本文中,我们描述了利用分离出的iNOS加氧酶和还原酶结构域来重建一氧化氮合成活性的过程。以不同比例混合这些结构域表明,L - 精氨酸不会产生一氧化氮,但反应中间体Nω - 羟基 - L - 精氨酸(L - NOHA)能够生成一氧化氮。在重建系统中,L - NOHA的表观米氏常数(Km)为100 μM,而天然iNOS的该常数为19 μM。D - NOHA不是底物。最大比活性(每血红素)出现在加氧酶与还原酶的摩尔比为4:1时,更高的比例会导致一定程度的抑制。活性的重建与结构域片段之间的电子转移相关,并导致加氧酶结构域血红素铁的不完全还原。L - NOHA而非L - 精氨酸会增加重建系统中NADPH的消耗。每由L - NOHA生成一个一氧化氮会消耗2.5至3.0个NADPH,这大大高于天然iNOS的化学计量比(每生成一个一氧化氮氧化0.5个NADPH),表明结构域片段之间存在解偶联的电子转移。因此,分离出的iNOS还原酶和加氧酶结构域各自保留了其独立的催化功能,但相互作用仅催化一氧化氮合成的第二步。(摘要截断于250字)

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