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髓鞘碱性蛋白与髓鞘特异性神经节苷脂GM4相互作用。

Myelin basic protein interacts with the myelin-specific ganglioside GM4.

作者信息

Mullin B R, Decandis F X, Montanaro A J, Reid J D

出版信息

Brain Res. 1981 Oct 5;222(1):218-21. doi: 10.1016/0006-8993(81)90963-x.

Abstract

Demyelinated plaques in multiple sclerosis have decreased amounts of both myelin basic protein and sialosylgalactosylceramide (GM4), a ganglioside specifically localized in myelin and oligodendroglia of the central nervous system. We have found that myelin basic protein is capable of releasing large quantities of entrapped [14C]glucose from multilamellar liposomes containing GM4. If the conformation of GM4 in liposomal membranes resembles that of GM4 in its natural environment, basic protein and GM4 may be associated within the myelin sheath of the central nervous system and their interaction altered in demyelinating diseases such as multiple sclerosis.

摘要

多发性硬化症中的脱髓鞘斑块中髓鞘碱性蛋白和唾液酸半乳糖神经酰胺(GM4,一种特异性定位于中枢神经系统髓鞘和少突胶质细胞的神经节苷脂)的含量均降低。我们发现髓鞘碱性蛋白能够从含有GM4的多层脂质体中释放大量被困的[14C]葡萄糖。如果脂质体膜中GM4的构象与其天然环境中的GM4构象相似,那么碱性蛋白和GM4可能在中枢神经系统的髓鞘内相互关联,并且它们的相互作用在诸如多发性硬化症等脱髓鞘疾病中会发生改变。

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