Jang K L, Collins M K, Latchman D S
Department of Biochemistry, University College and Middlesex School of Medicine, London, U.K.
J Acquir Immune Defic Syndr (1988). 1992;5(11):1142-7.
The HIV Tat protein is able to upregulate the transcription by RNA polymerase III of cotransfected or endogenous cellular Alu-repeated sequences in both HeLa and Jurkat T cells. This effect is mediated by an increase in the activity of transcription factor TFIIIC, which binds to the B box in the RNA polymerase III Alu promoter. This is the first example of an effect of the Tat protein on the transcription of a cellular gene or on the activity of a cellular transcription factor. The significance of this effect for the life cycle of HIV and its interaction with infected cells is discussed.
HIV反式激活因子(Tat蛋白)能够上调RNA聚合酶III对共转染的或内源性细胞Alu重复序列的转录,该过程在HeLa细胞和Jurkat T细胞中均会发生。这种效应是由转录因子TFIIIC的活性增加介导的,TFIIIC可与RNA聚合酶III的Alu启动子中的B框结合。这是Tat蛋白对细胞基因转录或细胞转录因子活性产生影响的首个实例。本文还讨论了这种效应对于HIV生命周期及其与受感染细胞相互作用的意义。