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人类免疫缺陷病毒tat蛋白通过增强细胞转录因子TFIIIC的活性来增加人类Alu重复序列的转录。

The human immunodeficiency virus tat protein increases the transcription of human Alu repeated sequences by increasing the activity of the cellular transcription factor TFIIIC.

作者信息

Jang K L, Collins M K, Latchman D S

机构信息

Department of Biochemistry, University College and Middlesex School of Medicine, London, U.K.

出版信息

J Acquir Immune Defic Syndr (1988). 1992;5(11):1142-7.

PMID:1403646
Abstract

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.

摘要

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。

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