Boldogh I, AbuBakar S, Deng C Z, Albrecht T
Department of Microbiology, University of Texas Medical Branch, Galveston 77550.
J Virol. 1991 Mar;65(3):1568-71. doi: 10.1128/JVI.65.3.1568-1571.1991.
The mechanisms responsible for the human cytomegalovirus (HCMV)-induced increase in cellular oncogene RNAs for c-jun, c-fos, and c-myc in human embryo lung cells (I. Boldogh, S. AbuBakar, and T. Albrecht, Science 247:561-564, 1990) were investigated. Results of transcription assays indicated that the rapid increase in RNA levels for the above-noted oncogenes was controlled at the transcriptional level and was related to enhanced transcription. The maximum rates of transcription for c-jun and c-fos genes occurred at 40 min postinfection, while for the c-myc gene the maximum rate occurred at about 60 min. The magnitude of HCMV-induced activation of these cellular genes was similar to the activation induced by serum. The half-lives of the cellular oncogenes showed similar decay rates after either serum or HCMV activation when measured by dactinomycin chase. The half-life for c-fos or c-jun was about 20 min, and that for c-myc was about 40 min. Furthermore, inhibition of the RNA increase by dactinomycin or by alpha-amanitin suggested that the increase in RNA levels was due to an increase in the transcriptional activity of oncogenes triggered by HCMV.
研究了人类巨细胞病毒(HCMV)诱导人胚肺细胞中c-jun、c-fos和c-myc细胞癌基因RNA增加的机制(I.博尔多格、S.阿布巴卡尔和T.阿尔布雷希特,《科学》247:561 - 564,1990)。转录分析结果表明,上述癌基因RNA水平的快速增加在转录水平受到调控,且与转录增强有关。c-jun和c-fos基因的最大转录速率在感染后40分钟出现,而c-myc基因的最大转录速率在约60分钟出现。HCMV诱导的这些细胞基因的激活程度与血清诱导的激活程度相似。当通过放线菌素追踪测量时,血清或HCMV激活后细胞癌基因的半衰期显示出相似的衰减速率。c-fos或c-jun的半衰期约为20分钟,c-myc的半衰期约为40分钟。此外,放线菌素或α-鹅膏蕈碱对RNA增加的抑制表明,RNA水平的增加是由于HCMV触发的癌基因转录活性增加所致。