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对日本莱施-奈恩综合征患者的次黄嘌呤-鸟嘌呤磷酸核糖转移酶基因分析

Hypoxanthine-guanine phosphoribosyltransferase gene analysis for Japanese patients with Lesch-Nyhan syndrome.

作者信息

Shimizu N, Konomi H, Arima M, Aoki T

机构信息

Second Department of Pediatrics, Ohashi Hospital, Toho University School of Medicine, Tokyo, Japan.

出版信息

Acta Paediatr Jpn. 1996 Feb;38(1):36-40. doi: 10.1111/j.1442-200x.1996.tb03432.x.

Abstract

The Lesch-Nyhan syndrome results as a consequence of a severe deficiency of functional activity of purine salvage enzyme, hypoxanthine phosphoribosyltransferase (HPRT). We performed Southern blot analysis for five patients and their families using full length cDNA of the HPRT gene as a probe. Pst I digested Southern blot analysis revealed a large deletion that included exon 2 in patient 3. The size of this deletion was about 4.4 Kb. The mother of this patient had the same mutated allele and a normal one (heterozygote). This type of mutation from a Lesch-Nyhan syndrome patient has not been previously reported. The restriction fragment length polymorphism (RFLP) pattern was analyzed by Bam HI digested Southern blot analysis for one family who had no major gene abnormality. We determined from this analysis that the sister of the patient was a Lesch-Nyhan syndrome carrier and the fetus (brother) was normal for HPRT activity. This study shows RFLP analysis is still useful for carrier detection and prenatal diagnosis of Lesch-Nyhan syndrome.

摘要

莱施-奈恩综合征是由于嘌呤补救酶次黄嘌呤磷酸核糖转移酶(HPRT)功能活性严重缺乏所致。我们使用HPRT基因的全长cDNA作为探针,对5名患者及其家族进行了Southern印迹分析。Pst I酶切的Southern印迹分析显示患者3存在一个包括外显子2的大片段缺失。该缺失大小约为4.4 kb。该患者的母亲有一个相同的突变等位基因和一个正常等位基因(杂合子)。这种来自莱施-奈恩综合征患者的突变类型此前未见报道。对一个无主要基因异常的家族进行了Bam HI酶切的Southern印迹分析,以分析限制性片段长度多态性(RFLP)模式。通过该分析我们确定患者的姐姐是莱施-奈恩综合征携带者,胎儿(弟弟)的HPRT活性正常。本研究表明RFLP分析对于莱施-奈恩综合征的携带者检测和产前诊断仍然有用。

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