Tang Nelson L S, Hui Joannie, Young Elisabeth, Worthington Viki, To Ka-Fai, Cheung Kam-Lau, Li Chi-Kong, Fok Tai-Fai
Department of Chemical Pathology, Faculty of Medicine, The Chinese University of Hong Kong, China.
Mol Genet Metab. 2003 Jun;79(2):142-5. doi: 10.1016/s1096-7192(03)00068-4.
We identified a novel mutation in the glycogen phosphorylase gene (PGYL) in a Chinese patient with glycogen storage disease (GSD) type VI. The patient presented with gross hepatomegaly since the age of two without history of any hypoglycemic attack. Otherwise, he was largely asymptomatic. Liver tissue enzyme assays revealed a mild deficiency of total glycogen phosphorylase. Both PGYL and PHKA2 genes were sequenced. The patient was homozygous of a missense mutation G233D in PGYL. This location forms a hairpin turn secondary structure and the small glycine residue is completely conserved in all the orthologous proteins from Escherichia coli to mammals. This is the sixth reported mutation of this form of GSD.
我们在中国一名患有VI型糖原贮积病(GSD)的患者中,鉴定出糖原磷酸化酶基因(PGYL)的一种新突变。该患者自两岁起出现肝脏明显肿大,无任何低血糖发作史。除此之外,他基本无症状。肝脏组织酶分析显示总糖原磷酸化酶轻度缺乏。对PGYL和PHKA2基因均进行了测序。该患者在PGYL基因上存在错义突变G233D的纯合子。此位置形成一个发夹状二级结构,并且从大肠杆菌到哺乳动物的所有直系同源蛋白中,小的甘氨酸残基都是完全保守的。这是该型GSD报道的第六个突变。