Hermans M M, Kroos M A, de Graaff E, Oostra B A, Reuser A J
Department of Cell Biology, Genetics and Clinical Genetics, Erasmus University, Rotterdam, The Netherlands.
Hum Mutat. 1993;2(4):268-73. doi: 10.1002/humu.1380020406.
The autosomal recessive glycogen storage disease type II is associated with a deficiency of lysosomal alpha-glucosidase (acid maltase). This paper reports on the mutations in the lysosomal alpha-glucosidase alleles of an adult patient. A G-1927 to A transition was discovered in exon 14 causing the substitution of Gly-643 by Arg and a second C-2173 to T transition in exon 15 resulting in the substitution of Arg-725 by Trp. Each of the mutations was located in a different allele. The mutations were introduced in the wild-type lysosomal alpha-glucosidase cDNA and expressed in COS cells. Both mutations had a similar effect. The synthesis of the mutant enzyme precursors was not disturbed but the intracellular transport and maturation were impaired. As a result there was an overall deficiency of catalytic activity.
常染色体隐性遗传的II型糖原贮积病与溶酶体α-葡萄糖苷酶(酸性麦芽糖酶)缺乏有关。本文报道了一名成年患者溶酶体α-葡萄糖苷酶等位基因的突变情况。在外显子14中发现了一个从G-1927到A的转换,导致Gly-643被Arg替代,在外显子15中发现了第二个从C-2173到T的转换,导致Arg-725被Trp替代。每个突变都位于不同的等位基因中。将这些突变引入野生型溶酶体α-葡萄糖苷酶cDNA并在COS细胞中表达。两种突变都有类似的效应。突变酶前体的合成未受干扰,但细胞内运输和成熟受损。结果导致催化活性总体缺乏。