Nakajima H
Second Department of Internal Medicine, Osaka University Medical School.
Nihon Rinsho. 1995 May;53(5):1241-6.
This review is aimed to provide the up-to-date knowledge on phosphofructokinase (PFK), a key enzyme of glycolysis, with special references to the recent advances of molecular biology of the enzyme. In human, three isozymes named M (muscle), L (liver) and P (platelet) are identified. Recently, mRNA and gene structures of these isozymes have been clarified. Deficiency of PFK-M is characterized by muscle weakness due to fuel crisis in exercising muscles. Up to now, gene defects of PFK deficient patients have been sought in 38 alleles from Japanese, Ashkenazi Jewish, Non-Ashkenazi Italian, French Canadian and Swiss patients and molecular heterogeneity has been elucidated. Down syndrome, in which trisomy of chromosome 21 is known provides us an interesting gene-dosage effect on PFK-L isozyme. Other various pathologic states affecting PFK activity in vivo are also reviewed briefly.
本综述旨在提供有关磷酸果糖激酶(PFK)(糖酵解的关键酶)的最新知识,并特别提及该酶分子生物学的最新进展。在人类中,已鉴定出三种同工酶,分别命名为M(肌肉型)、L(肝脏型)和P(血小板型)。最近,这些同工酶的mRNA和基因结构已得到阐明。PFK-M缺乏的特征是由于运动肌肉中的能量危机导致肌肉无力。到目前为止,已在来自日本、德系犹太人、非德系意大利人、法裔加拿大人和瑞士患者的38个等位基因中寻找PFK缺乏患者的基因缺陷,并阐明了分子异质性。已知21号染色体三体的唐氏综合征为我们提供了关于PFK-L同工酶有趣的基因剂量效应。还简要综述了体内影响PFK活性的其他各种病理状态。