Murakami Y, Satake M, Yamaguchi-Iwai Y, Sakai M, Muramatsu M, Ito Y
Department of Viral Oncology, Kyoto University, Japan.
Proc Natl Acad Sci U S A. 1991 May 1;88(9):3947-51. doi: 10.1073/pnas.88.9.3947.
Polyomavirus (Py) DNA replication is regulated by its enhancer, which contains an AP1 site, c-Jun and c-Fos, the products of nuclear protooncogenes c-jun and c-fos, form the heterodimeric transcriptional activating factor AP1. Overexpression of c-fos and c-jun genes strongly stimulated Py DNA replication from the Py origin of replication as well as transcription from the Py early promoter through the AP1 binding site. The cAMP response element (CRE)-binding protein CREB stimulated only transcription, not DNA replication, through the CRE under similar conditions. The results indicate that AP1 functions as a regulator of DNA replication and that the mechanism of activation of Py DNA replication by AP1 is distinct from that of activation of transcription from the Py early promoter.
多瘤病毒(Py)DNA复制受其增强子调控,该增强子含有一个AP1位点,核原癌基因c-jun和c-fos的产物c-Jun和c-Fos形成异二聚体转录激活因子AP1。c-fos和c-jun基因的过表达强烈刺激了来自Py复制起点的Py DNA复制以及通过AP1结合位点从Py早期启动子的转录。在相似条件下,cAMP反应元件(CRE)结合蛋白CREB仅通过CRE刺激转录,而非DNA复制。结果表明AP1作为DNA复制的调节因子,且AP1激活Py DNA复制的机制不同于其激活Py早期启动子转录的机制。