Hug G, Schubert W K, Chuck G
Science. 1966 Sep 23;153(3743):1534-5. doi: 10.1126/science.153.3743.1534.
Studies of a child with glycogenosis revealed an increased concentration of glycogen and low phosphorylase activity in her liver. Using mixtures of homogenates of the patient's liver and of normal liver, we found the low phosphorylase activity to be caused by a deficiency of phosphorylase kinase and not of hepatic phosphorylase. The fact that phosphorylase activity was restored to normal values by the addition of phosphorylase b kinase from rabbit muscle substantiates this conclusion.
对一名糖原贮积病患儿的研究显示,其肝脏中糖原浓度升高且磷酸化酶活性降低。通过使用该患者肝脏匀浆与正常肝脏匀浆的混合物,我们发现低磷酸化酶活性是由磷酸化酶激酶缺乏而非肝磷酸化酶缺乏所致。通过添加来自兔肌肉的磷酸化酶b激酶可使磷酸化酶活性恢复至正常水平,这一事实证实了该结论。