Nakamura M, Niki M, Nagata K, Ohtani K, Saito S, Hinuma Y, Sugamura K
Department of Microbiology, Tohoku University School of Medicine, Sendai, Japan.
J Biol Chem. 1989 Dec 5;264(34):20189-92.
The trans-acting transcriptional factor p40tax of human T-cell leukemia virus type I (HTLV-I) can activate expression not only of its own viral genes but also of other viral and cellular genes. We examined the cis-acting sequences in the simian virus 40 (SV40) enhancer required for its activation by HTLV-I p40tax. Experiments with chloramphenicol acetyltransferase constructs bearing the SV40 enhancer elements revealed that p40tax-dependent transactivation of the SV40 enhancer is mediated through the C element that contains the typical sequence for binding of a nuclear factor NF-kappa B. Activation of the C element by p40tax was seen in a limited set of cell lines as was also seen with the whole enhancer of SV40. Binding of NF-kappa B or NF-kappa B-like factor to the SV40 C element increased when p40tax was expressed. The fact that HTLV-I p40tax utilizes a cellular regulatory mechanism to transactivate the SV40 enhancer in a cell-dependent manner may have implications for the pathogenesis of adult T-cell leukemia.
人类I型T细胞白血病病毒（HTLV-I）的反式作用转录因子p40tax不仅可以激活其自身病毒基因的表达，还能激活其他病毒和细胞基因的表达。我们研究了猿猴病毒40（SV40）增强子中被HTLV-I p40tax激活所需的顺式作用序列。对携带SV40增强子元件的氯霉素乙酰转移酶构建体进行的实验表明，SV40增强子的p40tax依赖性反式激活是通过C元件介导的，该元件包含核因子NF-κB结合的典型序列。与SV40的整个增强子一样，在有限的一组细胞系中观察到p40tax对C元件的激活。当表达p40tax时，NF-κB或NF-κB样因子与SV40 C元件的结合增加。HTLV-I p40tax利用细胞调节机制以细胞依赖性方式反式激活SV40增强子这一事实可能对成人T细胞白血病的发病机制具有重要意义。
