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Xylosyl- and glucuronyltransferase functions of LARGE in α-dystroglycan modification are conserved in LARGE2.LARGE 中木糖基转移酶和葡萄糖醛酸基转移酶在α-肌营养不良蛋白修饰中的作用在 LARGE2 中是保守的。
Glycobiology. 2013 Mar;23(3):295-302. doi: 10.1093/glycob/cws152. Epub 2012 Nov 2.
2
O-Mannosylation and human disease.O-甘露糖基化与人类疾病。
Cell Mol Life Sci. 2013 Aug;70(16):2849-57. doi: 10.1007/s00018-012-1193-0. Epub 2012 Nov 1.
3
DPM2-CDG: a muscular dystrophy-dystroglycanopathy syndrome with severe epilepsy.DPM2-CDG：一种伴有严重癫痫的肌肉营养不良症- dystroglycanopathy 综合征。
Ann Neurol. 2012 Oct;72(4):550-8. doi: 10.1002/ana.23632.
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Exome sequencing and functional validation in zebrafish identify GTDC2 mutations as a cause of Walker-Warburg syndrome.外显子组测序和功能验证在斑马鱼中发现 GTDC2 突变是 Walker-Warburg 综合征的一个原因。
Am J Hum Genet. 2012 Sep 7;91(3):541-7. doi: 10.1016/j.ajhg.2012.07.009.
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Mouse fukutin deletion impairs dystroglycan processing and recapitulates muscular dystrophy.鼠 FKRP 缺失导致 dystroglycan 加工受损，重现肌肉营养不良。
J Clin Invest. 2012 Sep;122(9):3330-42. doi: 10.1172/JCI63004. Epub 2012 Aug 27.
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Developmental expression of the neuron-specific N-acetylglucosaminyltransferase Vb (GnT-Vb/IX) and identification of its in vivo glycan products in comparison with those of its paralog, GnT-V.神经元特异性 N-乙酰氨基葡萄糖转移酶 Vb（GnT-Vb/IX）的发育表达及其体内糖基产物与同工酶 GnT-V 的比较鉴定。
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8
Glycosylation of α-dystroglycan: O-mannosylation influences the subsequent addition of GalNAc by UDP-GalNAc polypeptide N-acetylgalactosaminyltransferases.α- 连接的岩藻糖基化聚糖：O- 岩藻糖基化影响随后 UDP-N-乙酰半乳糖胺：多肽 N-乙酰半乳糖胺基转移酶添加 GalNAc。
J Biol Chem. 2012 Jun 15;287(25):20967-74. doi: 10.1074/jbc.M112.370387. Epub 2012 May 1.
9
Mutations in ISPD cause Walker-Warburg syndrome and defective glycosylation of α-dystroglycan.ISPD 基因突变会导致沃克-沃伯格综合征和α- dystroglycan 的糖基化缺陷。
Nat Genet. 2012 May;44(5):581-5. doi: 10.1038/ng.2253.
10
ISPD loss-of-function mutations disrupt dystroglycan O-mannosylation and cause Walker-Warburg syndrome.ISPD 功能丧失突变会破坏 dystroglycan 的 O-甘露糖基化，并导致 Walker-Warburg 综合征。
Nat Genet. 2012 May;44(5):575-80. doi: 10.1038/ng.2252.

O-甘露糖基化途径：糖基转移酶和与先天性肌营养不良症相关的蛋白。

The o-mannosylation pathway: glycosyltransferases and proteins implicated in congenital muscular dystrophy.

机构信息

Complex Carbohydrate Research Center and Department of Biochemistry and Molecular Biology, University of Georgia, Athens, Georgia 30602, USA.

出版信息

J Biol Chem. 2013 Mar 8;288(10):6930-5. doi: 10.1074/jbc.R112.438978. Epub 2013 Jan 17.

DOI:10.1074/jbc.R112.438978
PMID:23329833
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3591603/
Abstract

Several forms of congenital muscular dystrophy, referred to as dystroglycanopathies, result from defects in the protein O-mannosylation biosynthetic pathway. In this minireview, I discuss 12 proteins involved in the pathway and how they play a role in the building of glycan structures (most notably on the protein α-dystroglycan) that allow for binding to multiple proteins of the extracellular matrix.

摘要

几种先天性肌肉萎缩症，称为 dystroglycanopathies，是由于蛋白 O-甘露糖基化生物合成途径的缺陷引起的。在这篇小综述中，我将讨论该途径涉及的 12 种蛋白以及它们在聚糖结构（尤其是在蛋白 α- dystroglycan 上）形成中所起的作用，这些聚糖结构允许与细胞外基质的多种蛋白结合。