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组成型小脑一氧化氮合酶双域结构的证据。

Evidence for a bidomain structure of constitutive cerebellar nitric oxide synthase.

作者信息

Sheta E A, McMillan K, Masters B S

机构信息

Department of Biochemistry, University of Texas Health Science Center, San Antonio 78284-7760.

出版信息

J Biol Chem. 1994 May 27;269(21):15147-53.

PMID:7515050
Abstract

Nitric oxide synthase (NOS) catalyzes the NADPH-dependent, Ca2+/calmodulin-dependent formation of NO and citrulline from L-arginine and molecular oxygen. The localization of the heme-binding consensus sequence in the NH2-terminal half of NOS and of the binding sequences for nucleotides (FMN and FAD) in the COOH-terminal half suggests a bidomain structure. In addition, the presence of a putative calmodulin-binding sequence between the heme- and flavin-binding domains of the enzyme suggests a role for calmodulin in modulating a spatial orientation of these domains that is required for catalytic activity. First, to determine the effects of calmodulin and the functionality of the separated domains, Ca2+/calmodulin binding-induced conformational changes in NOS were measured by fluorescence quenching, from which a binding constant of approximately 1 nM for calmodulin was calculated. Second, electron transport to various artificial acceptors was measured. The addition of Ca2+/calmodulin increased cytochrome c reduction from 10-15-fold while stimulating the rate of 2,6-dichlorophenolindophenol and ferricyanide reduction only slightly, if at all. Calmodulin stimulation of NOS results in NADPH-mediated cytochrome c reduction, which is sensitive to superoxide dismutase, and the reduction of acetylated cytochrome c, which is only weakly reducible by unstimulated NOS. Thus, this stimulated activity is presumably superoxide anion-mediated. Third, limited proteolysis of NOS in the absence of calmodulin resulted in a time-dependent increase in cytochrome c reductase activity, which was not inhibitable by superoxide dismutase, and a decrease in catalysis of NO formation. SDS-polyacrylamide gel electrophoresis analysis of the tryptic digest demonstrated the formation of approximately 89- and approximately 79-kDa fragments. Sequence analysis of the peptides confirmed that trypsin cleaves the enzyme in the putative calmodulin-binding region beginning with Ala728. This region was protected from proteolysis by the addition of Ca2+/calmodulin. The separated NH2-terminal domain exhibited the characteristic spectrum of bound heme, while the COOH-terminal domain showed the characteristic spectrum of bound flavins. Other cleavage patterns were obtained in the presence of calmodulin. The data demonstrate that the heme- and flavin-binding domains of NOS can be isolated in functionally intact forms.

摘要

一氧化氮合酶(NOS)催化L-精氨酸和分子氧在NADPH依赖、Ca2+/钙调蛋白依赖的条件下生成NO和瓜氨酸。NOS氨基末端一半区域中血红素结合共有序列的定位以及羧基末端一半区域中核苷酸(FMN和FAD)结合序列的定位表明其具有双结构域结构。此外,在该酶的血红素结合域和黄素结合域之间存在一个假定的钙调蛋白结合序列,这表明钙调蛋白在调节这些结构域的空间取向中发挥作用,而这种空间取向是催化活性所必需的。首先,为了确定钙调蛋白的作用以及分离结构域的功能,通过荧光猝灭测量了Ca2+/钙调蛋白结合诱导的NOS构象变化,据此计算出钙调蛋白的结合常数约为1 nM。其次,测量了向各种人工受体的电子传递。添加Ca2+/钙调蛋白使细胞色素c还原增加了10 - 15倍,而对2,6 - 二氯酚靛酚和铁氰化物还原速率的刺激(如果有的话)则很轻微。钙调蛋白对NOS的刺激导致NADPH介导的细胞色素c还原,这对超氧化物歧化酶敏感,以及乙酰化细胞色素c的还原,未受刺激的NOS对其还原作用较弱。因此,这种受刺激的活性可能是由超氧阴离子介导的。第三,在没有钙调蛋白的情况下对NOS进行有限的蛋白酶解,导致细胞色素c还原酶活性随时间增加,这不受超氧化物歧化酶抑制,同时NO生成的催化作用降低。对胰蛋白酶消化产物进行SDS - 聚丙烯酰胺凝胶电泳分析表明形成了约89 kDa和约79 kDa的片段。对肽段的序列分析证实胰蛋白酶在假定的钙调蛋白结合区域从Ala⁷²⁸开始切割该酶。通过添加Ca2+/钙调蛋白可保护该区域不被蛋白酶解。分离的氨基末端结构域呈现出结合血红素的特征光谱,而羧基末端结构域呈现出结合黄素的特征光谱。在存在钙调蛋白的情况下获得了其他切割模式。数据表明NOS 的血红素结合域和黄素结合域可以以功能完整的形式分离出来。

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