Brain gangliosides in axon-myelin stability and axon regeneration

被引:115
作者
Schnaar, Ronald L. [1 ,2 ]
机构
[1] Johns Hopkins Sch Med, Dept Pharmacol & Mol Sci, Baltimore, MD 21205 USA
[2] Johns Hopkins Sch Med, Dept Neurosci, Baltimore, MD 21205 USA
基金
美国国家卫生研究院;
关键词
Ganglioside; Myelin; Myelin-associated glycoprotein; Axon regeneration; Lectin; LACKING COMPLEX GANGLIOSIDES; NEURITE OUTGROWTH INHIBITION; RAT-BRAIN; DEVELOPMENTAL-CHANGES; NERVE REGENERATION; RECEPTOR FUNCTION; GLYCOPROTEIN; MICE; GM3; BINDING;
D O I
10.1016/j.febslet.2009.10.011
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Gangliosides, sialic acid-bearing glycosphingolipids, are expressed at high abundance and complexity in the brain. Altered ganglioside expression results in neural disorders, including seizures and axon degeneration. Brain gangliosides function, in part, by interacting with a ganglioside-binding lectin, myelin-associated glycoprotein (MAG). MAG, on the innermost wrap of the myelin sheath, binds to gangliosides GD1a and GT1b on axons. MAG-ganglioside binding ensures optimal axon-myelin cell-cell interactions, enhances long-term axon-myelin stability and inhibits axon outgrowth after injury. Knowledge of the molecular interactions of brain gangliosides may improve understanding of axon-myelin stability and provide opportunities to enhance recovery after nerve injury. (C) 2009 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
引用
收藏
页码:1741 / 1747
页数:7
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