Maekawa T, Matsuda S, Fujisawa J, Yoshida M, Ishii S
Laboratory of Molecular Genetics, Tsukuba Life Science Center, Institute of Physical and Chemical Research (RIKEN), Ibaraki, Japan.
Oncogene. 1991 Apr;6(4):627-32.
The adenovirus E1A protein and tax protein (Tax) of human T-cell leukemia virus-1 (HTLV-1) are transcriptional regulators that do not bind to DNA directly. The ATF sites/CRE (cyclic AMP response element) of the adenovirus E4 promoter and the long terminal repeat of HTLV-1 have been shown to be required for E1A and Tax inducibility, respectively. Using the c-Myb-CRE-BP1 fusion protein, it was shown that CRE-BP1, which could bind to the ATF sites/CRE, mediated the E1A-induced trans-activation. For this activation, the N-terminal portion of CRE-BP1, which contained the putative metal finger structure, was essential but not sufficient. In contrast, the trans-activation induced by HTLV-1 Tax was not mediated by CRE-BP1. These results strongly suggested that E1A activates transcription through interaction with CRE-BP1, but another CRE-binding protein participates in the Tax-induced trans-activation.
腺病毒E1A蛋白和人类T细胞白血病病毒1型（HTLV-1）的Tax蛋白是不直接与DNA结合的转录调节因子。腺病毒E4启动子的ATF位点/CRE（环磷酸腺苷反应元件）和HTLV-1的长末端重复序列已分别被证明是E1A和Tax诱导活性所必需的。使用c-Myb-CRE-BP1融合蛋白，研究表明，能够与ATF位点/CRE结合的CRE-BP1介导了E1A诱导的反式激活。对于这种激活，包含推定金属指结构的CRE-BP1的N末端部分是必不可少的，但并不充分。相反，HTLV-1 Tax诱导的反式激活不是由CRE-BP1介导的。这些结果强烈表明，E1A通过与CRE-BP1相互作用激活转录，但另一种CRE结合蛋白参与了Tax诱导的反式激活。
