Activation of the HTLV-I long terminal repeat by the hepatitis B virus X protein.
Activation of the HTLV-I long terminal repeat by the hepatitis B virus X protein.
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乙型肝炎病毒 X 蛋白激活 HTLV-I 长末端重复序列。
DOI：
10.1006/viro.1996.0522
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Butel,JS
中科院分区：
文献类型：
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作者：
Marriott,SJ;Lee,TH;Slagle,BL;Butel,JS
人T细胞白血病病毒I型（HTLV-I）Tax蛋白和B肝炎病毒（HBV）X蛋白已显示各自激活其各自的病毒启动子以及细胞基因启动子的子集的转录。在这里，我们表明，HTLV-Ⅰ长末端重复序列（LTR）是响应HBV X的反式激活。X介导的LTR反式激活的最大水平为8倍。LTR的X响应区（XRR）位于核苷酸-355和-276之间，包含AP-2结合位点，这是一个先前识别的X响应元件。我们证明Tax和X协同激活HTLV-I LTR的转录，尽管AP-2结合位点对于这种协同作用不是必需的。这些结果提高了HBV X蛋白可能影响合并感染个体中HTLV-I基因表达水平的可能性。
The human T-cell leukemia virus type I (HTLV-I) Tax protein and the hepatitis B virus (HBV) X protein have each been shown to activate transcription of their respective viral promoters as well as a subset of cellular gene promoters. Here we show that the HTLV-I long terminal repeat (LTR) is responsive to HBV X transactivation. Maximum levels of X-mediated transactivation of the LTR were 8-fold. An X-responsive-region (XRR) of the LTR is located between nucleotides −355 and −276 and contains an AP-2 binding site, a previously recognized X-responsive element. We demonstrated that Tax and X synergize to activate transcription from the HTLV-I LTR, although the AP-2 binding site was not required for this synergy. These results raise the possibility that the HBV X protein may affect the level of HTLV-I gene expression in co-infected individuals.