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构建了不同长度人免疫缺陷病毒LTR启动子的荧光酶报告基因(Luc)表达质粒;瞬时转染Jurkat细胞;同时与含tat基因的表达质粒pCVI共转染;通过荧光酶活性的测定,分析Tat与LTR对基因表达的作用机制。实验结果表明LTR—158上游区有负调控元件的存在;证实了Tat的反式激活作用可以大大提高LTR指导的基因表达水平;研究结果揭示LTR中的增强子序列及其结合蛋白NF—kB在高水平的LTR转录以及Tat的反式激活作用中可能起重要作用。
The luciferase reporter gene (Luc) expression plasmid of LTR promoter of different length human immunodeficiency virus was constructed; transiently transfected into Jurkat cells; cotransfected with the expression vector pCVI containing the tat gene; the luciferase activity assay was used to analyze Tat And LTR on gene expression mechanism. The results showed that there was a negative regulatory element in the upstream of LTR-158. It was confirmed that the transactivation of Tat can greatly improve the gene expression level guided by LTR. The results revealed that the enhancer sequence and its binding protein NF-kB in LTR High levels of LTR transcription and Tat transactivation may play an important role.