Seliger B, Kruppa G, Schäfer R, Redmond S M, Pfizenmaier K
Clinical Research Group Biological Regulation of Host-Tumor Interaction, Max Planck Society, University of Göttingen, Federal Republic of Germany.
J Virol. 1988 Feb;62(2):619-21. doi: 10.1128/JVI.62.2.619-621.1988.
In transformed NIH 3T3 cells, murine gamma interferon reduces the expression of the long terminal repeat-controlled oncogenes v-mos, c-myc, and v-Ha-ras by a direct effect on the activity of retroviral promoters, as revealed by analyses of RNA half-life and transcriptional activity of retroviral genes as well as by analyses of chloramphenicol acetyltransferase activity in cells transformed with the cat gene under the control of long terminal repeats.
在转化的NIH 3T3细胞中,小鼠γ干扰素通过直接影响逆转录病毒启动子的活性,降低长末端重复序列控制的癌基因v-mos、c-myc和v-Ha-ras的表达,这一结果通过对RNA半衰期、逆转录病毒基因转录活性的分析以及对在长末端重复序列控制下用cat基因转化的细胞中氯霉素乙酰转移酶活性的分析得以揭示。