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CACNA1A基因的新发突变导致乙酰唑胺反应性发作性共济失调。

De novo mutation in CACNA1A caused acetazolamide-responsive episodic ataxia.

作者信息

Yue Q, Jen J C, Thwe M M, Nelson S F, Baloh R W

机构信息

Department of Neurology, UCLA School of Medicine, Los Angeles, California 90095-1769, USA.

出版信息

Am J Med Genet. 1998 May 26;77(4):298-301. doi: 10.1002/(sici)1096-8628(19980526)77:4<298::aid-ajmg9>3.0.co;2-j.

Abstract

With the recent report of mutations in the calcium channel gene CACNA1A in two families with episodic ataxia type 2, we investigated a patient with nonfamilial episodic vertigo and ataxia responsive to acetazolamide for similar mutations. Single-strand conformation polymorphism (SSCP) analysis of exon 23 identified an extra band in the patient that was not present in other relatives or in normal controls. Exon 23 of the patient showed a spontaneous C to T substitution at position 4410 resulting in an early stop codon. Patients with nonfamilial episodic ataxia may respond to acetazolamide and may have mutations in CACNA1A.

摘要

随着最近有报道称,在两个患有发作性共济失调2型的家族中,钙通道基因CACNA1A发生了突变,我们对一名患有非家族性发作性眩晕且对乙酰唑胺有反应的共济失调患者进行了研究,以寻找类似的突变。对第23外显子进行单链构象多态性(SSCP)分析时,在该患者中发现了一条额外的条带,而在其他亲属或正常对照中并未出现。该患者的第23外显子在第4410位发生了自发的C到T替换,导致出现一个提前终止密码子。非家族性发作性共济失调患者可能对乙酰唑胺有反应,且可能存在CACNA1A突变。

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