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瑞典的软骨发育不全由成纤维细胞生长因子受体3(FGFR3)中的G1138A突变引起。

Achondroplasia in Sweden caused by the G1138A mutation in FGFR3.

作者信息

Alderborn A, Anvret M, Gustavson K H, Hagenäs L, Wadelius C

机构信息

Department of Clinical Genetics, University Hospital, Uppsala, Sweden.

出版信息

Acta Paediatr. 1996 Dec;85(12):1506-7. doi: 10.1111/j.1651-2227.1996.tb13963.x.

Abstract

Achondroplasia, an autosomal dominant inherited disorder, is one of the most common forms of skeletal dysplasia resulting in disproportionate extreme shortness. Recently, two point mutations, both affecting nucleotide 1138 in the fibroblast growth factor receptor type 3 (FGFR3) gene, were found to be the cause of the disorder. We investigated DNA from 16 Swedish patients with achondroplasia for the presence of these mutations. All patients were found to be heterozygous for the G to A transition at nucleotide 1138. Our data thus support previous reports showing a striking genetic homogeneity, in that almost all achondroplasia patients have the FGFR3 G380R mutation at the protein level.

摘要

软骨发育不全是一种常染色体显性遗传性疾病,是导致身材极度不成比例矮小的最常见骨骼发育异常形式之一。最近,发现两个均影响成纤维细胞生长因子受体3(FGFR3)基因中第1138位核苷酸的点突变是该疾病的病因。我们对16名瑞典软骨发育不全患者的DNA进行了检测,以确定这些突变的存在情况。所有患者均被发现第1138位核苷酸处存在G到A的转换杂合子。因此,我们的数据支持了之前的报告,即显示出显著的基因同质性,因为几乎所有软骨发育不全患者在蛋白质水平上都有FGFR3 G380R突变。

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