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β-淀粉样蛋白与过氧化氢酶高亲和力结合并抑制过氧化氢分解。

Amyloid-beta binds catalase with high affinity and inhibits hydrogen peroxide breakdown.

作者信息

Milton N G

机构信息

Department of Molecular Pathology, Royal Free and University College Medical School, University College London, Royal Free Campus, Rowland Hill Street, London NW3 2PF, U.K.

出版信息

Biochem J. 1999 Dec 1;344 Pt 2(Pt 2):293-6.

PMID:10567208
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1220643/
Abstract

Amyloid-beta (Abeta) specifically bound purified catalase with high affinity and inhibited catalase breakdown of H(2)O(2). The Abeta-induced catalase inhibition involved formation of the inactive catalase Compound II and was reversible. Catalase<-->Abeta interactions provide rapid functional assays for the cytotoxic domain of Abeta and suggest a mechanism for some of the observed actions of Abeta plus catalase in vitro.

摘要

β淀粉样蛋白(Aβ)以高亲和力特异性结合纯化的过氧化氢酶,并抑制过氧化氢酶对H₂O₂的分解。Aβ诱导的过氧化氢酶抑制作用涉及无活性的过氧化氢酶化合物II的形成,且是可逆的。过氧化氢酶与Aβ的相互作用为Aβ的细胞毒性结构域提供了快速功能测定方法,并提示了体外观察到的Aβ加过氧化氢酶某些作用的机制。

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本文引用的文献

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The A beta peptide of Alzheimer's disease directly produces hydrogen peroxide through metal ion reduction.阿尔茨海默病的Aβ肽通过金属离子还原直接产生过氧化氢。
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Binding of beta-amyloid to the p75 neurotrophin receptor induces apoptosis. A possible mechanism for Alzheimer's disease.β-淀粉样蛋白与p75神经营养因子受体的结合会诱导细胞凋亡。这是阿尔茨海默病的一种可能机制。
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An intracellular protein that binds amyloid-beta peptide and mediates neurotoxicity in Alzheimer's disease.一种与β淀粉样肽结合并在阿尔茨海默病中介导神经毒性的细胞内蛋白质。
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Rapid cellular uptake of Alzheimer amyloid betaA4 peptide by cultured human neuroblastoma cells.培养的人神经母细胞瘤细胞对阿尔茨海默病β淀粉样蛋白A4肽的快速细胞摄取。
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Analysis of heterogeneous A4 peptides in human cerebrospinal fluid and blood by a newly developed sensitive Western blot assay.通过新开发的灵敏蛋白质印迹分析法分析人脑脊液和血液中的异质A4肽。
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Amyloid beta-protein reduces acetylcholine synthesis in a cell line derived from cholinergic neurons of the basal forebrain.β-淀粉样蛋白可降低源自基底前脑胆碱能神经元的细胞系中的乙酰胆碱合成。
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