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腺苷脱氨酶缺乏症的分子基础。

Molecular basis of adenosine deaminase deficiency.

作者信息

Markert M L

机构信息

Duke University, Medical Center, Durham, NC 27710.

出版信息

Immunodeficiency. 1994;5(2):141-57.

PMID:8032366
Abstract

Adenosine deaminase (ADA) deficiency is an autosomal recessive disorder resulting in immunodeficiency. Since the cDNA for ADA was cloned approximately 10 years ago, investigators have determined the molecular basis for disease in many patients with ADA deficiency. Mutations that have been identified include point mutations causing amino acid substitutions, premature stop codons, RNA splicing errors, and deletion mutations. Approximately one third of patients are homozygous for their mutation; in some of these cases the parents are known to be related. One mutation, Ala329-Val, is the most common, being present in 8 of the 21 ADA-deficient SCID patients whose mutations have been reported.

摘要

腺苷脱氨酶(ADA)缺乏症是一种导致免疫缺陷的常染色体隐性疾病。自从大约10年前克隆出ADA的互补DNA(cDNA)以来,研究人员已经确定了许多ADA缺乏症患者的疾病分子基础。已发现的突变包括导致氨基酸替代的点突变、过早的终止密码子、RNA剪接错误和缺失突变。大约三分之一的患者其突变是纯合的;在其中一些病例中,已知父母有亲缘关系。一种突变,即丙氨酸329缬氨酸突变是最常见的,在已报告突变情况的21例ADA缺陷型重症联合免疫缺陷(SCID)患者中有8例存在该突变。

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