Beutler E, Westwood B, Melemed A, Dal Borgo P, Margolis D
Department of Molecular and Experimental Medicine, Scripps Research Institute, La Jolla, CA 92037, USA.
Blood Cells Mol Dis. 1995;21(1):64-72. doi: 10.1006/bcmd.1995.0010.
Three previously undescribed mutations of the glucose-6-phosphate dehydrogenase (G6PD) gene have been documented in patients with hereditary non-spherocytic hemolytic anemia (HNSHA). In none of the cases have we been able to obtain a sufficient volume of blood to characterize the residual enzyme biochemically. "G6PD Calvo Mackenna" was due to an A-->G transition in cDNA nucleotide 1138 creating an Aat II site and resulting in a substitution of valine for isoleucine at amino acid 380. "G6PD Riley" was due to a T-->C transition at cDNA nucleotide 1139 also changing the 380 isoleucine, in this case to a threonine. "G6PD Wisconsin" was due to an C-->G transversion in cDNA nucleotide 1177, destroying a Aci I site and resulting in a substitution of glycine for arginine at amino acid 393. All of these mutations were in exon 10, where mutations that cause HNSHA appear to be clustered. We present a list of the 83 mutations of G6PD that have been documented to the end of April, 1995.
在遗传性非球形红细胞溶血性贫血(HNSHA)患者中,已发现葡萄糖-6-磷酸脱氢酶(G6PD)基因的三种先前未描述的突变。在所有病例中,我们都未能获得足够量的血液以对残留酶进行生化特性分析。“G6PD 卡尔沃·麦肯纳”是由于cDNA核苷酸1138处的A→G转换,产生了一个Aat II位点,并导致氨基酸380处的异亮氨酸被缬氨酸取代。“G6PD 莱利”是由于cDNA核苷酸1139处的T→C转换,同样改变了380位的异亮氨酸,在这种情况下变为苏氨酸。“G6PD 威斯康星”是由于cDNA核苷酸1177处的C→G颠换,破坏了一个Aci I位点,并导致氨基酸393处的精氨酸被甘氨酸取代。所有这些突变都在外显子10中,导致HNSHA的突变似乎聚集在此处。我们列出了截至1995年4月底已记录的83种G6PD突变。