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佩利措伊斯-梅茨巴赫样综合征患者中M6b基因的突变分析。

Mutation analysis of the M6b gene in patients with Pelizaeus-Merzbacher-like syndrome.

作者信息

Henneke Marco, Wehner Lars-Erik, Hennies Hans Christian, Preuss Natalie, Gärtner Jutta

机构信息

Department of Pediatrics and Pediatric Neurology, Georg August University, Göttingen, Germany.

出版信息

Am J Med Genet A. 2004 Jul 15;128A(2):156-8. doi: 10.1002/ajmg.a.30068.

Abstract

"Pelizaeus-Merzbacher-like syndrome" is an undetermined leukodystrophy disorder of diffuse hypomyelination. The patients' clinical phenotype is indistinguishable from classical Pelizaeus-Merzbacher disease (PMD), but the patients lack PLP1 gene duplications or mutations. They represent about 20% of all cases with a clinical PMD phenotype. The M6b gene has been localized to Xp22.2. The encoded M6B protein is a member of a novel proteolipid family that also includes other major brain myelin components like the proteolipid protein (PLP). Recent cotransfection experiments suggest a protein-protein interaction of M6B and mutant PLP1 that may contribute to oligodendrocyte dysfunction in PMD. Therefore, M6b has been considered a good candidate gene for Pelizaeus-Merzbacher-like syndrome. However, our molecular analyses in eight thoroughly characterized patients make it unlikely that mutations in this gene are involved in this subgroup of human hypomyelination disorders.

摘要

“佩利措伊斯-梅茨巴赫样综合征”是一种弥漫性髓鞘形成不良的未明性脑白质营养不良症。患者的临床表型与经典的佩利措伊斯-梅茨巴赫病(PMD)无法区分,但患者缺乏PLP1基因重复或突变。他们约占所有具有临床PMD表型病例的20%。M6b基因已定位到Xp22.2。编码的M6B蛋白是一个新的蛋白脂质家族的成员,该家族还包括其他主要的脑髓鞘成分,如蛋白脂质蛋白(PLP)。最近的共转染实验表明,M6B与突变型PLP1之间存在蛋白质-蛋白质相互作用,这可能导致PMD中少突胶质细胞功能障碍。因此,M6b被认为是佩利措伊斯-梅茨巴赫样综合征的一个良好候选基因。然而,我们对八名特征明确的患者进行的分子分析表明,该基因的突变不太可能与人类髓鞘形成不良症的这一亚组有关。

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