INDUCTION OF THE HTLV-I LTR BY JUN OCCURS THROUGH THE TAX-RESPONSIVE 21-BP ELEMENTS
INDUCTION OF THE HTLV-I LTR BY JUN OCCURS THROUGH THE TAX-RESPONSIVE 21-BP ELEMENTS
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DOI：
10.1016/0042-6822(91)90487-v
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发表时间：
1991-03-01
期刊：
影响因子：
3.7
通讯作者：
KIM, SJ
中科院分区：
文献类型：
--
作者：
JEANG, KT;CHIU, R;KIM, SJ
HTLV-I LTR已知可由多种细胞信号诱导。Tax蛋白是一种有效的ltr定向转录病毒反式激活剂。我们在这里证明了Jun是另一个可以强烈调节该LTR活性的转录因子。通过删除和竞争研究，发现Jun激活的LTR的最小部分与税收响应的21-bp元件一致。在结合实验中，与HTLV-I 21-bp序列结合的核因子被过量的AP-1基序寡核苷酸竞争。尽管税收响应元件不包含严格保守的AP-1基序，但这些发现表明它们具有AP-1位点的功能。然而，我们发现，在AP-1活性缺失的细胞（F9畸胎癌）中，HTLV-I LTR的Tax激活得以维持。因此，虽然Jun/AP-1可能参与HTLV-I LTR的基础表达，但它可能不是税收介导的激活所必需的。
The HTLV-I LTR is known to be induced by a variety of cellular signals. Tax protein is one potent viral trans-activator of LTR-directed transcription. We demonstrate here that Jun is another transcription factor that can strongly modulate the activity of this LTR. Using deletion and competition studies, the minimal portion of the LTR for Jun activation was found to coincide with the Tax-responsive 21-bp elements. In binding experiments, nuclear factors that bound to the HTLV-I 21-bp sequence were competed by an excess of AP-1 motif oligonucleotide. Although the Tax-responsive elements do not contain a strictly conserved AP-1 motif, these findings suggest that they function as AP-1 sites. We found, however, that in cells depleted for AP-1 activity (F9 teratocarcinoma), Tax activation of the HTLV-I LTR was maintained. Thus while Jun/AP-1 may be involved in the basal expression of the HTLV-I LTR, it may not be essential for Tax-mediated activation.