脂蛋白脂肪酶基因外显子3的移码突变导致过早终止密码子和脂蛋白脂肪酶缺乏。

Molecular biology & medicine Pub Date : 1990-12-01
H E Henderson, R Devlin, J Peterson, J D Brunzell, M R Hayden
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引用次数: 0

摘要

人类脂蛋白脂肪酶(LPL)基因的几个突变已被证明是LPL缺乏的基础。这些突变主要发生在欧洲血统的患者中,包括导致过早终止密码子的单碱基转移,四个独立的氨基酸替换和两个大的基因重排。在该实验室检测的50名患者的DNA中,这两种基因约占LPL等位基因的40%。我们现在报告一个新的突变在LPL基因外显子3从东南亚提取的南非受试者。该突变包括在单个碱基缺失位点上插入六个碱基对。在102 ~ 103个氨基酸位置净插入5个碱基对导致阅读框移位,产生44个随机序列氨基酸残基,并在第4外显子内产生一个过早终止密码子。这种突变预计会导致合成一种明显截断的蛋白质,这是导致我们的病人酶缺乏的原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Frameshift mutation in exon 3 of the lipoprotein lipase gene causes a premature stop codon and lipoprotein lipase deficiency.

Several mutations in the human lipoprotein lipase (LPL) gene have been shown to underlie LPL deficiency. These mutations occur in patients who are mainly of European descent, and comprise a single base transition causing a premature stop codon, four separate amino acid substitutions and two large gene rearrangements. Together they account for approximately 40% of the LPL alleles in a cohort of 50 patients whose DNA has been examined in this laboratory. We now report on a new mutation in exon 3 of the LPL gene from a South African subject of South-east Asian extraction. This mutation comprises a six base-pair insertion at the site of a single base deletion. The net insertion of five base-pairs at amino acid positions 102 to 103 causes a shift in the reading frame, generating 44 amino acid residues of random sequence and a premature stop codon within exon 4. This mutation is predicted to result in the synthesis of a markedly truncated protein and is the cause of the enzyme deficiency in our patient.

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