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在一个患有X连锁遗传性铁粒幼细胞贫血的大家族中,鉴定出红细胞5-氨基酮戊酸合成酶基因中第452位精氨酸被组氨酸取代。

Identification of an arginine452 to histidine substitution in the erythroid 5-aminolaevulinate synthetase gene in a large pedigree with X-linked hereditary sideroblastic anaemia.

作者信息

Edgar A J, Losowsky M S, Noble J S, Wickramasinghe S N

机构信息

Department of Haematology, Imperial College of Medicine at St Mary's, London, UK.

出版信息

Eur J Haematol. 1997 Jan;58(1):1-4. doi: 10.1111/j.1600-0609.1997.tb01402.x.

Abstract

The coding region of the erythroid 5-aminolaevulinate synthetase gene (ALAS2) from a large pedigree with pyridoxine-responsive X-linked hereditary sideroblastic anaemia was examined for mutations. In three affected males from this pedigree, single strand conformational polymorphism (SSCP) analysis showed anomalous migration of a PCR product spanning exon 9. Sequencing of amplified genomic DNA from one of these affected males revealed a guanine to adenine transition at nucleotide 1407 of the cDNA sequence in exon 9 of the gene. This mutation results in the loss of an HhaI restriction enzyme digest site. An HhaI digest assay demonstrated the presence of this mutation in other affected males but not in unaffected males and unrelated individuals. The point mutation results in an arginine to histidine substitution at amino acid residue 452. The arginine residue is conserved in both the erythroid and housekeeping ALAS genes in all known vertebrate sequences. This arginine is located in the middle of a predicted alpha-helix.

摘要

对一个患有吡哆醇反应性X连锁遗传性铁粒幼细胞贫血的大家系的红系5-氨基乙酰丙酸合成酶基因(ALAS2)编码区进行了突变检测。在该家系的三名患病男性中,单链构象多态性(SSCP)分析显示跨越外显子9的PCR产物迁移异常。对其中一名患病男性的扩增基因组DNA进行测序,发现在该基因外显子9的cDNA序列第1407位核苷酸处发生了鸟嘌呤到腺嘌呤的转变。这种突变导致HhaI限制性内切酶消化位点的缺失。HhaI消化试验表明该突变存在于其他患病男性中,但不存在于未患病男性和无关个体中。该点突变导致氨基酸残基452处的精氨酸被组氨酸取代。在所有已知脊椎动物序列中,精氨酸残基在红系和管家ALAS基因中都是保守的。该精氨酸位于预测的α螺旋中间。

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