Krietsch W K, Krietsch H, Kaiser W, Dünnwald M, Kuntz G W, Duhm J, Bücher T
Eur J Clin Invest. 1977 Oct;7(5):427-35. doi: 10.1111/j.1365-2362.1977.tb01630.x.
An X-chromosome linked phosphoglycerate kinase deficiency in erythrocytes and leucocytes was discovered in a large German kindred. Seven males of two generations were found to have only 21% of the normal enzyme activity in their erythrocytes, and twelve females of three generations showed various degrees of this defect. The differences in the expression of the deficiency in heterozygote females are explained by the Lyon hypothesis. The deficiency is caused by a variant enzyme, named phosphoglycerate kinase München. Although it differs from the normal enzyme electrophoretically, the two enzymes resemble one another closely in many respects. They have essentially the same Km for the substrates of the backward reaction, identical pH optima and similar rates of thermal inactivation. In contrast to the nine previously described phosphoglycerate kinase deficiencies, all of which are associated with haemolytic anaemia, the carriers of phosphoglycerate kinase München show no overt clinical symptoms. The erythrocyte concentrations of adenine nucleotides and 2,3-diphosphoglycerate are normal.
在一个德国大家族中发现了一种红细胞和白细胞中与X染色体连锁的磷酸甘油酸激酶缺乏症。两代中的7名男性红细胞中的酶活性仅为正常水平的21%,三代中的12名女性表现出不同程度的这种缺陷。杂合子女性中该缺乏症表达的差异可用莱昂假说解释。该缺乏症由一种变异酶引起,名为慕尼黑磷酸甘油酸激酶。尽管它在电泳上与正常酶不同,但这两种酶在许多方面非常相似。它们对逆向反应底物的米氏常数基本相同,最适pH相同,热失活速率相似。与之前描述的9种磷酸甘油酸激酶缺乏症不同,所有这些缺乏症都与溶血性贫血有关,而慕尼黑磷酸甘油酸激酶的携带者没有明显的临床症状。红细胞中腺嘌呤核苷酸和2,3-二磷酸甘油酸的浓度正常。