Tan T H, Jia R, Roeder R G
Laboratory of Biochemistry and Molecular Biology, Rockefeller University, New York, New York 10021-6399.
J Virol. 1989 Sep;63(9):3761-8. doi: 10.1128/JVI.63.9.3761-3768.1989.
The human T-cell leukemia virus type I (HTLV-I) trans-activator (tax)-inducible enhancer was localized to three copies of 21-base-pair repeats within the long terminal repeat. Interestingly, the TGACG motif found in the center of the 21-base-pair tax-responsive element (TRE) is also present in the cyclic AMP (cAMP)-responsive elements (CREs) and activating transcription factor (ATF)-binding sites. In this study, we demonstrate that the three TRE-binding proteins, TREB-1, TREB-2, and TREB-3, also bind to various CREs and ATF-binding sites and that the TREs can confer upon a heterologous promoter responsiveness to various inducing agents, including tax, cAMP, and E1a. Furthermore, the transcriptional activation of the HTLV-I promoter by tax can be inhibited by several protein kinase inhibitors, including sangivamycin. Our results indicate that the TREs, CREs, and ATF-binding sites are similar cis-acting elements and further suggest (i) that the transcriptional activation of the HTLV-I promoter by tax involves the action of a protein kinase and (ii) that induction by tax, cAMP, and E1a might be mediated by distinct factors or kinases.
人类I型T细胞白血病病毒（HTLV-I）反式激活因子（tax）诱导的增强子定位于长末端重复序列内的三个21碱基对重复序列。有趣的是，在21碱基对tax反应元件（TRE）中心发现的TGACG基序也存在于环磷酸腺苷（cAMP）反应元件（CRE）和激活转录因子（ATF）结合位点中。在本研究中，我们证明三种TRE结合蛋白TREB-1、TREB-2和TREB-3也能结合各种CRE和ATF结合位点，并且TRE可赋予异源启动子对包括tax、cAMP和E1a在内的各种诱导剂的反应性。此外，tax对HTLV-I启动子的转录激活可被包括放线菌素在内的几种蛋白激酶抑制剂抑制。我们的结果表明，TRE、CRE和ATF结合位点是相似的顺式作用元件，并进一步表明：（i）tax对HTLV-I启动子的转录激活涉及蛋白激酶的作用；（ii）tax、cAMP和E1a的诱导可能由不同的因子或激酶介导。
