Barth M L, Fensom A, Harris A
Division of Medical and Molecular Genetics, UMDS-Guy's Campus, London, UK.
Hum Genet. 1993 Mar;91(1):73-7. doi: 10.1007/BF00230227.
The frequency of two common disease-associated mutations in the arylsulphatase A (ASA) gene, and of a mutation causing ASA pseudodeficiency, have been established in metachromatic leukodystrophy patients diagnosed in our laboratory. A total of 37 mutant genes have been analysed. The G-->A change destroying the splice donor site of exon 2 is generally associated with more severe disease and was found in 43.2% of mutant ASA genes. The C-->T transition causing a proline to leucine substitution at position 426 in exon 8 (P426-->L) is associated with later onset disease, and was found in 16.2% of mutant genes. The A-->G transition leading to loss of a polyadenylation signal associated with ASA pseudodeficiency was present at a frequency of 7.5% in the patients and heterozygotes studied.
在我们实验室诊断的异染性脑白质营养不良患者中,已确定了芳基硫酸酯酶A(ASA)基因中两种常见疾病相关突变以及一种导致ASA假性缺乏的突变的频率。共分析了37个突变基因。破坏外显子2剪接供体位点的G→A变化通常与更严重的疾病相关,在43.2%的突变ASA基因中被发现。导致外显子8第426位脯氨酸替换为亮氨酸(P426→L)的C→T转换与疾病较晚发病相关,在16.2%的突变基因中被发现。导致与ASA假性缺乏相关的多聚腺苷酸化信号缺失的A→G转换在所研究的患者和杂合子中的频率为7.5%。