Suppr超能文献

FBN1基因的c.7409G>A(p.Cys2470Tyr)变异:三代人的表型变异性

The c.7409G>A (p.Cys2470Tyr) Variant of FBN1: Phenotypic Variability across Three Generations.

作者信息

Potter K J, Creighton S, Armstrong L, Eydoux P, Duncan W, Penny D J, Fan Y, Gibson W T

机构信息

Department of Pathology and Laboratory Medicine, University of British Columbia, B.C., Canada ; Department of Child and Family Research Institute, University of British Columbia, B.C., Canada.

出版信息

Mol Syndromol. 2013 Mar;4(3):125-35. doi: 10.1159/000347163. Epub 2013 Feb 28.

Abstract

Marfan syndrome is an autosomal dominant connective tissue disorder caused by mutations in the fibrillin gene FBN1, which encodes an extracellular matrix glycoprotein. Major features of Marfan syndrome occur in the ocular, cardiovascular, and skeletal systems as well as in the dura mater. Approximately 60% of known disease-causing mutations are missense mutations of single amino acid residues. Effects on the cardiovascular system are classically associated with mutations in exons 24-32 of the 65 FBN1 exons and many, though not all, reports associate missense mutations in exons 59-65 with a mild cardiovascular phenotype. Here we present 5 related individuals among whom a c.7409G>A (p.Cys2470Tyr) missense variant in exon 59 of FBN1 is associated with significant cardiovascular features. The index case also had an apparently de novo 46,XX,del(5)(q33.1q33.3) deletion on chromosome 5. This family demonstrates skeletal, dermatological and neurological features consistent with Marfan syndrome but lacks significant ophthalmological findings to date. These findings suggest that FBN1 C-terminal missense mutations may not confer the ophthalmological features of Marfan syndrome, but they also confer a more significant risk for cardiovascular pathology than that suggested by previous studies. Furthermore, clinical data from this family supports the previously reported association of dural ectasia with C-terminal mutations.

摘要

马凡综合征是一种常染色体显性遗传性结缔组织疾病,由原纤维蛋白基因FBN1突变引起,该基因编码一种细胞外基质糖蛋白。马凡综合征的主要特征出现在眼、心血管、骨骼系统以及硬脑膜。大约60%已知的致病突变是单个氨基酸残基的错义突变。对心血管系统的影响通常与FBN1的65个外显子中第24 - 32外显子的突变有关,许多(尽管不是全部)报告将第59 - 65外显子中的错义突变与轻度心血管表型相关联。在此,我们报告了5名相关个体,其中FBN1第59外显子中的一个c.7409G>A(p.Cys2470Tyr)错义变异与显著的心血管特征相关。先证者还在5号染色体上有一个明显的新发46,XX,del(5)(q33.1q33.3)缺失。这个家系表现出与马凡综合征一致的骨骼、皮肤和神经特征,但迄今为止缺乏显著的眼科表现。这些发现表明,FBN1 C末端错义突变可能不会赋予马凡综合征的眼科特征,但它们也会带来比先前研究表明的更大的心血管病变风险。此外,这个家系的临床数据支持了先前报道的硬脊膜膨出与C末端突变的关联。

相似文献

本文引用的文献

2
The revised Ghent nosology for the Marfan syndrome.修订版马凡综合征根特分类法。
J Med Genet. 2010 Jul;47(7):476-85. doi: 10.1136/jmg.2009.072785.
5
Subluxation of lens in Marfan syndrome.
Indian Pediatr. 2009 May;46(5):434.
10
Marfan syndrome-diagnosis and management.马凡综合征的诊断与管理。
Curr Probl Cardiol. 2008 Jan;33(1):7-39. doi: 10.1016/j.cpcardiol.2007.10.001.

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验