Hiraki Y, Garcia de Herreros A, Birnbaum M J
Department of Cellular and Molecular Physiology, Harvard Medical School, Boston, MA 02115.
Proc Natl Acad Sci U S A. 1989 Nov;86(21):8252-6. doi: 10.1073/pnas.86.21.8252.
The rat brain glucose transporter (GT) gene is rapidly activated coincident with the initiation of growth in response to oncogenic transformation or the addition of growth factors to quiescent fibroblasts. The latter response has been shown to be mediated by protein kinase C-dependent and-independent pathways. We studied the role of protein kinase C in the transformation-induced activation of the GT gene. Transformation of fibroblasts by either the v-fps or the Ki-ras oncogene rapidly increased the levels of GT mRNA. Either viral oncogene remained capable of stimulating the GT gene after depletion of cellular protein kinase C by prolonged pretreatment of fibroblasts with phorbol 12-myristate 13-acetate. These data indicate that protein kinase C is not required for the rapid activation of gene transcription by oncogenic transformation.
大鼠脑葡萄糖转运体(GT)基因在致癌转化或向静止的成纤维细胞添加生长因子后,随着生长的启动而迅速被激活。后一种反应已被证明是由蛋白激酶C依赖性和非依赖性途径介导的。我们研究了蛋白激酶C在转化诱导的GT基因激活中的作用。用v-fps或Ki-ras癌基因转化成纤维细胞会迅速增加GT mRNA的水平。在用佛波醇12-肉豆蔻酸酯13-乙酸盐对成纤维细胞进行长时间预处理以耗尽细胞蛋白激酶C后,任何一种病毒癌基因仍能够刺激GT基因。这些数据表明,致癌转化快速激活基因转录不需要蛋白激酶C。