Fujisawa J, Toita M, Yoshida M
Department of Viral Oncology, Cancer Institute, Tokyo, Japan.
J Virol. 1989 Aug;63(8):3234-9. doi: 10.1128/JVI.63.8.3234-3239.1989.
The trans activator (p40tax) of human T-cell leukemia virus type I (HTLV-I) is a transcriptional factor that activates the long terminal repeat (LTR) of HTLV-I and interleukin-2 receptor alpha. We examined the HTLV-I enhancer responsible for tax-mediated trans activation and identified (A/T)(G/C)(G/C)CNNTGACG(T/A) as a plausible tax-responsive element (TRE). The putative TRE in the LTR was found to be different from the elements required for activation by cycle AMP and 12-O-tetradecanoylphorbol-13-acetate, although these elements overlapped each other. The TRE was also different from a binding site of an NF-kappa B-like factor that was identified in the interleukin-2 receptor alpha promoter and human immunodeficiency virus LTR as a TRE. The latter result was further demonstrated by the failure of the NF-kappa B sequence to compete with the TRE of the LTR in a protein-binding assay. These findings indicate that tax function and its cascade can modulate activities of various enhancer sequences, which are probably regulated by distinct DNA-binding factors.
人类I型T细胞白血病病毒(HTLV-I)的反式激活因子(p40tax)是一种转录因子,可激活HTLV-I的长末端重复序列(LTR)和白细胞介素-2受体α。我们研究了负责tax介导的反式激活的HTLV-I增强子,并确定(A/T)(G/C)(G/C)CNNTGACG(T/A)为可能的tax反应元件(TRE)。尽管这些元件相互重叠,但发现LTR中的推定TRE与环磷酸腺苷和12-O-十四烷酰佛波醇-13-乙酸酯激活所需的元件不同。TRE也不同于在白细胞介素-2受体α启动子和人类免疫缺陷病毒LTR中作为TRE鉴定的NF-κB样因子的结合位点。蛋白质结合试验中NF-κB序列无法与LTR的TRE竞争,进一步证明了后一结果。这些发现表明,tax功能及其级联反应可以调节各种增强子序列的活性,这些增强子序列可能由不同的DNA结合因子调控。