替换为精氨酸甘氨酸- 213 extracellular-superoxide歧化酶损害亲和力肝素和内皮细胞表面。
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足立T,山田H,山田Y, Morihara N,山崎N,村上T,普天间基地,加藤K, Hirano K
替换为精氨酸甘氨酸- 213 extracellular-superoxide歧化酶损害亲和力肝素和内皮细胞表面。
j . 1996 1月1;313 (Pt (1): 235 - 9。
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8546689 (在PubMed]
- 文摘
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Extracellular-superoxide歧化酶(EC-SOD)在血清水平分为两个不连续组:一个低级别的组低于400 ng / ml,高级组高于400 ng / ml(足立,中村,山田,普天间基地,加藤和Hirano(1994)中国。詹。229年学报,123 - 131]。分子遗传研究表明,高级组的捐助者单个碱基替换为精氨酸生成甘氨酸的交换- 213 (R213G) heparin-binding EC-SOD域()、尼尔森、Karlsson和Marklund(1994)生物。化学。269年,19163 - 19166;山田、山田、足立,Goto,小笠原群岛,普天间基地,北野,Hirano和加藤(1995)日本。j .的嗡嗡声。麝猫。40,177 - 184]。血清EC-SOD水平比杂合子和纯合子主题明显高于正常人。血清EC-SOD从杂合子以及该同样减少肝素亲和,根据heparin-HPLC,相比于正常的捐助者。 This result suggests that the serum EC-SOD in heterozygotes was mainly composed of the mutant form which has reduced heparin affinity. On the other hand, fibroblast cells derived from heterozygote subjects generated mRNA of both normal and mutant EC-SOD (m-EC-SOD), and expressed the corresponding proteins. EC-SOD is a tetrameric enzyme, and in heterozygote donors would be heterogeneous with regard to the constitution of normal and mutant subunits. The enzyme form consisting of only mutant subunits, the form with the weakest heparin affinity, can be preferentially driven out to the plasma phase, because EC-SOD in the vasculature exists in equilibrium between plasma and the endothelial cell surface. The binding of m-EC-SOD to bovine aortic endothelial cells was about 50-fold less than that of normal EC-SOD. This result suggests that the binding of m-EC-SOD to vascular endothelial cells is much decreased in vivo, which causes a high level of serum EC-SOD.