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溶酶体糖脂贮积症。

Lysosomal Glycosphingolipid Storage Diseases.

机构信息

LIMES Institute, Membrane Biology and Lipid Biochemistry Unit, Universität Bonn, D-53121 Bonn, Germany; email:

出版信息

Annu Rev Biochem. 2019 Jun 20;88:461-485. doi: 10.1146/annurev-biochem-013118-111518.

Abstract

Glycosphingolipids are cell-type-specific components of the outer leaflet of mammalian plasma membranes. Gangliosides, sialic acid-containing glycosphingolipids, are especially enriched on neuronal surfaces. As amphi-philic molecules, they comprise a hydrophilic oligosaccharide chain attached to a hydrophobic membrane anchor, ceramide. Whereas glycosphingolipid formation is catalyzed by membrane-bound enzymes along the secretory pathway, degradation takes place at the surface of intralysosomal vesicles of late endosomes and lysosomes catalyzed in a stepwise fashion by soluble hydrolases and assisted by small lipid-binding glycoproteins. Inherited defects of lysosomal hydrolases or lipid-binding proteins cause the accumulation of undegradable material in lysosomal storage diseases (GM1 and GM2 gangliosidosis; Fabry, Gaucher, and Krabbe diseases; and metachromatic leukodystrophy). The catabolic processes are strongly modified by the lipid composition of the substrate-carrying membranes, and the pathological accumulation of primary storage compounds can trigger an accumulation of secondary storage compounds (e.g., small glycosphingolipids and cholesterol in Niemann-Pick disease).

摘要

糖脂是哺乳动物质膜外层的细胞类型特异性成分。神经节苷脂是含有唾液酸的糖脂,特别丰富于神经元表面。作为两亲性分子,它们由连接在疏水性膜锚定物神经酰胺上的亲水寡糖链组成。虽然糖脂的形成是由沿着分泌途径的膜结合酶催化的,但降解发生在晚期内体囊泡和溶酶体的表面,由可溶性水解酶逐步催化,并由小的脂质结合糖蛋白辅助。溶酶体水解酶或脂质结合蛋白的遗传缺陷导致溶酶体贮积病(GM1 和 GM2 神经节苷脂病;法布里病、戈谢病和 Krabbe 病;和异染性脑白质营养不良)中不可降解物质的积累。代谢过程强烈受到携带底物的膜的脂质组成的影响,并且初级贮存化合物的病理性积累会引发次级贮存化合物的积累(例如尼曼-匹克病中的小糖脂和胆固醇)。

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