Goodman S A, Esau B, Koontz J W
Department of Biochemistry, University of Tennessee, Knoxville 37996-0840.
Arch Biochem Biophys. 1988 Nov 1;266(2):343-50. doi: 10.1016/0003-9861(88)90266-4.
Reuber H35 rat hepatoma cells respond to insulin or to tumor promoting phorbol esters with an increase in ornithine decarboxylase enzyme activity. This occurs in a time- and dose-dependent manner with both types of agonist. We report here that the increase in ornithine decarboxylase activity with optimal concentrations of both agonists is additive. Furthermore, the initial increase is dependent on continued RNA and protein synthesis. We also find that both of these agonists cause an increase in mRNA coding for ornithine decarboxylase in a time- and dose-dependent manner which suggests that the increase in enzyme activity can be accounted for by the increase in transcript levels. The difference in the time course of induction by the agonists, the additivity of induction by the two agonists, the differential sensitivity of induction to cycloheximide and RNA synthesis inhibitors, and the observation that phorbol myristic acetate causes a further increase in ornithine decarboxylase activity and transcript levels in cells already maximally induced by insulin suggest that these two agonists act through separate mechanisms.
鲁伯H35大鼠肝癌细胞对胰岛素或促肿瘤佛波酯的反应是鸟氨酸脱羧酶活性增加。两种激动剂都以时间和剂量依赖性方式引发这种情况。我们在此报告，两种激动剂的最佳浓度所引起的鸟氨酸脱羧酶活性增加是相加的。此外，最初的增加依赖于持续的RNA和蛋白质合成。我们还发现，这两种激动剂都以时间和剂量依赖性方式导致编码鸟氨酸脱羧酶的mRNA增加，这表明酶活性的增加可以由转录水平的增加来解释。激动剂诱导的时间进程差异、两种激动剂诱导的相加性、诱导对环己酰亚胺和RNA合成抑制剂的不同敏感性，以及肉豆蔻酸佛波酯在已被胰岛素最大程度诱导的细胞中导致鸟氨酸脱羧酶活性和转录水平进一步增加的观察结果表明，这两种激动剂通过不同的机制起作用。
