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IVA型黏多糖贮积症:N-乙酰半乳糖胺-6-硫酸酯酶基因突变的筛查与鉴定

Mucopolysaccharidosis IVA: screening and identification of mutations of the N-acetylgalactosamine-6-sulfate sulfatase gene.

作者信息

Ogawa T, Tomatsu S, Fukuda S, Yamagishi A, Rezvi G M, Sukegawa K, Kondo N, Suzuki Y, Shimozawa N, Orü T

机构信息

Department of Pediatrics, Gifu University School of Medicine, Japan.

出版信息

Hum Mol Genet. 1995 Mar;4(3):341-9. doi: 10.1093/hmg/4.3.341.

Abstract

Mutations causing mucopolysaccharidosis IVA in 15 Japanese and one Caucasian patient were characterized. To screen these mutations, we used a combination of single strand conformation polymorphism analysis and heteroduplex analysis for PCR products of targeted cDNA or genomic DNA. Various small mutations were identified in 23 of 26 alleles, while the other six alleles had large rearrangements. Cycle sequencing of PCR products revealed 15 different mutations, including 12 missense, one nonsense, one frame shift (2 bp deletion) and one splice site mutation, in accord with the broad range of clinical phenotypes. Two alleles have different mutations in the same nucleotide position of exon 3 (R94C, CGC-->TGC; R94G, CGC-->GGC), diagnosed by sequencing and by allelic-specific oligohybridization (ASO). One allele had two amino acid changes, E450V in exon 12 and V488M in exon 13, thereby indicating a double point mutation. All 16 mutations reported were confirmed by restriction enzyme assay or by allelic-specific oligohybridization. Transfection of mutagenized cDNAs into patients' fibroblasts showed that all mutations caused completely deficient or markedly decreased N-acetylgalactosamine-6-sulfate sulfatase (GALNS) activity, thereby indicating that these mutations were responsible for the enzyme deficiency.

摘要

对15名日本患者和1名高加索患者中导致IVA型粘多糖贮积症的突变进行了特征分析。为筛选这些突变,我们对靶向cDNA或基因组DNA的PCR产物采用了单链构象多态性分析和异源双链分析相结合的方法。在26个等位基因中的23个中鉴定出各种小突变,而其他6个等位基因有大片段重排。PCR产物的循环测序揭示了15种不同的突变,包括12个错义突变、1个无义突变、1个移码突变(2 bp缺失)和1个剪接位点突变,这与广泛的临床表型一致。通过测序和等位基因特异性寡核苷酸杂交(ASO)诊断,两个等位基因在第3外显子的相同核苷酸位置有不同突变(R94C,CGC→TGC;R94G,CGC→GGC)。一个等位基因有两个氨基酸变化,第12外显子中的E450V和第13外显子中的V488M,从而表明是双点突变。所有报道的16种突变均通过限制性酶切分析或等位基因特异性寡核苷酸杂交得到证实。将诱变的cDNA转染到患者成纤维细胞中表明,所有突变均导致N - 乙酰半乳糖胺 - 6 - 硫酸酯酶(GALNS)活性完全缺乏或显著降低,从而表明这些突变是酶缺乏的原因。

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