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细胞色素P450c17极端C末端的K494_V495缺失加R496L以及D487_F489缺失的新型复合杂合突变导致17α-羟化酶缺乏症。

A novel compound heterozygous mutation of K494_V495 deletion plus R496L and D487_F489 deletion in extreme C-terminus of cytochrome P450c17 causes 17alpha-hydroxylase deficiency.

作者信息

Lee Long-Shyong, Shu Wei-Jane, Wu Chen-Ming, Hsieh Chia-Hsing, Chen Su-Mei, Hu Chaur-Jong, Chen Wei-Yi, Chung Bon-Chu

机构信息

Department of Clinical Pathology, Jen-Ai Branch, Taipei City Hospital, Taipei, Taiwan.

出版信息

Mol Cell Endocrinol. 2006 Apr 25;249(1-2):16-20. doi: 10.1016/j.mce.2006.01.003. Epub 2006 Feb 17.

Abstract

17alpha-Hydroxylase deficiency is a rare disease caused by mutation of the CYP17 gene, resulting in hypertension, hypokalemia, female sexual infantilism or male pseudohermaphroditism, low blood cortisol and low plasma renin activity. Herein, we report a female Taiwanese with 17alpha-hydroxylase deficiency. The CYP17 genes of this patient and five members of her family were analyzed by PCR-direct sequencing. One allele of the patient contains a 9-bp (c. 1459-1467 GACTCTTTC: D487, S488, F489) deletion, which is prevalent in Southeast Asia. The other allele has a 6-bp (c. 1480-1485 AAGGTG: K494, V495) deletion and an R496L (c. 1487 G>T) missense mutation, which is a novel mutation. Site-directed mutagenesis, in vitro expression and functional analysis in HEK-293T cells showed that this novel mutation [K494_V495 Del; R496L] resulted in complete loss of 17alpha-hydroxylase and 17,20-lyase activity. Thus this novel mutation in the extreme C-terminus abolishes enzyme activity, and when accompanied by a 9-bp deletion at codons 487-489 in the other allele, results in 17alpha-hydroxylase/17,20-lyase deficiency in this patient.

摘要

17α-羟化酶缺乏症是一种由CYP17基因突变引起的罕见疾病,会导致高血压、低钾血症、女性性幼稚症或男性假两性畸形、血皮质醇降低和血浆肾素活性降低。在此,我们报告一名患有17α-羟化酶缺乏症的台湾女性。通过PCR直接测序分析了该患者及其家族五名成员的CYP17基因。患者的一个等位基因包含一个9碱基对(c. 1459 - 1467 GACTCTTTC:D487、S488、F489)缺失,这在东南亚地区较为常见。另一个等位基因有一个6碱基对(c. 1480 - 1485 AAGGTG:K494、V495)缺失和一个R496L(c. 1487 G>T)错义突变,这是一个新的突变。定点诱变、体外表达及在HEK - 293T细胞中的功能分析表明,这个新突变[K494_V495 Del;R496L]导致17α-羟化酶和17,20-裂解酶活性完全丧失。因此,极端C末端的这个新突变消除了酶活性,并且当另一个等位基因的第487 - 489密码子处伴有一个9碱基对缺失时,导致该患者出现17α-羟化酶/17,20-裂解酶缺乏症。

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