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I型干扰素对SV40早期转录的诱导作用。

Induction of SV40 early transcription by type I interferon.

作者信息

Tzen C Y, Scott R E

机构信息

Department of Pathology, University of Tennessee Medical Center, Memphis 38163.

出版信息

Exp Cell Res. 1993 Apr;205(2):246-50. doi: 10.1006/excr.1993.1083.

Abstract

Interferons (IFN) have cancer suppressor activities for many transformed cells; however, IFN does not suppress transformation by SV40 large T antigen. The studies described in this paper therefore evaluated the effect of IFN on SV40-promoted gene expression in 3T3T cells. The results show that SV40-promoted gene expression can be induced 200% or three-fold by Type I IFN treatment regardless of whether beta-galactosidase or chloramphenicol acetyltransferase (CAT) is used as the reporter gene. This IFN effect is dosage-dependent, requires 24-48 h of exposure for maximum induction of CAT activity, and is probably not due to a post-transcriptional effect of IFN on CAT because IFN has no effect on CAT expression driven by thymidine kinase promoter. The induction of SV40 early transcription by IFN does, however, require that the integration of plasmid within the cell's genome. Additional data specifically show that the SV40 promoter is required for IFN's effect because IFN will not induce CAT if the SV40 enhancer is inserted upstream of thymidine kinase promoter to control expression of CAT gene.

摘要

干扰素(IFN)对许多转化细胞具有癌症抑制活性;然而,IFN并不能抑制SV40大T抗原诱导的转化。因此,本文所述的研究评估了IFN对3T3T细胞中SV40促进的基因表达的影响。结果表明,无论使用β-半乳糖苷酶还是氯霉素乙酰转移酶(CAT)作为报告基因,I型IFN处理均可使SV40促进的基因表达诱导200%或增加三倍。这种IFN效应是剂量依赖性的,需要24 - 48小时的暴露才能最大程度地诱导CAT活性,并且这可能不是由于IFN对CAT的转录后效应,因为IFN对由胸苷激酶启动子驱动的CAT表达没有影响。然而,IFN诱导SV40早期转录确实需要质粒整合到细胞基因组中。其他数据具体表明,IFN的作用需要SV40启动子,因为如果将SV40增强子插入胸苷激酶启动子上游以控制CAT基因的表达,IFN将不会诱导CAT。

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