Zhao L J, Giam C Z
Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH 44106.
Proc Natl Acad Sci U S A. 1991 Dec 15;88(24):11445-9. doi: 10.1073/pnas.88.24.11445.
The human T-cell lymphotrophic virus type I (HTLV-I) Tax protein activates transcription from three 21-base-pair (bp) repeat sequences in the viral enhancer. Using gel electrophoretic mobility-shift assays, we now show that Tax interacts directly with the nuclear proteins, Tax activation factors (TAFs), that bind the 21-bp repeats. This interaction is demonstrated by decreased electrophoretic mobilities of the TAFs-21-bp-repeats complexes upon supply of Tax exogenously. Formation of the TAFs-21-bp-repeats and Tax-TAFs-21-bp-repeats complexes correlates with in vivo transactivation by Tax. Furthermore, interaction of Tax with TAFs enhances their binding to the 21-bp repeats. These data indicate that trans-activation by Tax is most likely mediated by interaction of Tax with TAFs.
人类I型嗜T细胞淋巴病毒(HTLV-I)的Tax蛋白可激活病毒增强子中三个21碱基对(bp)重复序列的转录。利用凝胶电泳迁移率变动分析,我们现在表明Tax可直接与结合21-bp重复序列的核蛋白——Tax激活因子(TAFs)相互作用。这种相互作用通过外源提供Tax时TAFs-21-bp重复序列复合物电泳迁移率降低得以证明。TAFs-21-bp重复序列复合物和Tax-TAFs-21-bp重复序列复合物的形成与Tax在体内的反式激活相关。此外,Tax与TAFs的相互作用增强了它们与21-bp重复序列的结合。这些数据表明,Tax的反式激活很可能是由Tax与TAFs的相互作用介导的。