Gregg R G, Wilce P A
Biochem Biophys Res Commun. 1983 Jul 29;114(2):473-8. doi: 10.1016/0006-291x(83)90804-5.
The reversible phosphorylation of microsomal 3-hydroxy-3-methylglutaryl CoA reductase in host liver and hepatoma 5123C has been investigated. The percentage of the total enzyme activity in vivo was similar in the normal liver, host liver and hepatoma 5123C. The inclusion of 30 mM EDTA and 10 mM mevalonic acid in assays of 3-hydroxy-3-methylglutaryl CoA reductase inactivation in vitro eliminated artifacts generated by the presence of mevalonate kinase. Inactivation of 3-hydroxy-3-methylglutaryl CoA reductase from normal liver, host liver and hepatoma occurred at a similar rate with similar half-times. We conclude that phosphorylation/dephosphorylation of 3-hydroxy-3-methylglutaryl CoA reductase occurs in hepatomas and that the lack of dietary cholesterol feedback inhibition in the hepatomas is not a result of a defect in this particular aspect of the reversible phosphorylation system.
对宿主肝脏和肝癌5123C中微粒体3-羟基-3-甲基戊二酰辅酶A还原酶的可逆磷酸化进行了研究。正常肝脏、宿主肝脏和肝癌5123C中体内总酶活性的百分比相似。在体外3-羟基-3-甲基戊二酰辅酶A还原酶失活测定中加入30 mM乙二胺四乙酸（EDTA）和10 mM甲羟戊酸消除了由甲羟戊酸激酶的存在产生的假象。来自正常肝脏、宿主肝脏和肝癌的3-羟基-3-甲基戊二酰辅酶A还原酶以相似的速率失活，半衰期相似。我们得出结论，3-羟基-3-甲基戊二酰辅酶A还原酶的磷酸化/去磷酸化发生在肝癌中，并且肝癌中缺乏膳食胆固醇反馈抑制不是可逆磷酸化系统这一特定方面存在缺陷的结果。
