Wagner S, Green M R
Program in Molecular Medicine, University of Massachusetts Medical Center, Worcester 01605.
Science. 1993 Oct 15;262(5132):395-9. doi: 10.1126/science.8211160.
The Tax protein of human T cell leukemia virus type-1 (HTLV-I) transcriptionally activates the HTLV-I promoter. This activation requires binding sites for activating transcription factor (ATF) proteins, a family of cellular proteins that contain basic region-leucine zipper (bZIP) DNA binding domains. Data are presented showing that Tax increases the in vitro DNA binding activity of multiple ATF proteins. Tax also stimulated DNA binding by other bZIP proteins, but did not affect DNA binding proteins that lack a bZIP domain. The increase in DNA binding occurred because Tax promotes dimerization of the bZIP domain in the absence of DNA, and the elevated concentration of the bZIP homodimer then facilitates the DNA binding reaction. These results help explain how Tax activates viral transcription and transforms cells.
人类嗜T细胞病毒1型(HTLV-I)的Tax蛋白可转录激活HTLV-I启动子。这种激活需要激活转录因子(ATF)蛋白的结合位点,ATF蛋白是一类含有碱性区域-亮氨酸拉链(bZIP)DNA结合结构域的细胞蛋白。本文给出的数据表明,Tax可增强多种ATF蛋白的体外DNA结合活性。Tax还能刺激其他bZIP蛋白的DNA结合,但不影响缺乏bZIP结构域的DNA结合蛋白。DNA结合活性的增加是因为Tax在无DNA的情况下促进bZIP结构域的二聚化,而bZIP同源二聚体浓度的升高进而促进了DNA结合反应。这些结果有助于解释Tax如何激活病毒转录并使细胞发生转化。