Hall D J, Alberta J A, Stiles C D
Dana Farber Cancer Institute, Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115.
Oncogene Res. 1989;4(3):177-84.
Platelet-derived growth factor (PDGF) stimulates the transcription of a number of genes in BALB/c-3T3 fibroblasts. Some of these genes (notably the c-myc and c-fo proto-oncogenes) are induced also by phorbol-based tumor promoters which activate protein kinase C. It appears that the response of these genes to PDGF is actually channeled through the activation of protein kinase C. However, other PDGF-inducible genes such as JE, KC, and JB do not respond to tumor promoter. Data suggest that a labile repressor protein blocks the transcriptional response of these genes to tumor promoter. This labile repressor is specific for elements in the JE, KC, and JB genes for it has no effect on the activation of the SV40 early promoter, which is a known target for phorbol ester-inducible transativation.
血小板衍生生长因子(PDGF)可刺激BALB/c - 3T3成纤维细胞中许多基因的转录。其中一些基因(特别是c - myc和c - fos原癌基因)也可被激活蛋白激酶C的佛波酯类肿瘤启动子所诱导。这些基因对PDGF的反应似乎实际上是通过蛋白激酶C的激活来传导的。然而,其他PDGF诱导基因,如JE、KC和JB,对肿瘤启动子没有反应。数据表明,一种不稳定的阻遏蛋白会阻断这些基因对肿瘤启动子的转录反应。这种不稳定的阻遏蛋白对JE、KC和JB基因中的元件具有特异性,因为它对SV40早期启动子的激活没有影响,而SV40早期启动子是佛波酯诱导的反式激活的已知靶点。