Transcriptional activation of the human immunodeficiency virus type 1 long terminal repeat by hepatitis B virus X-protein requires de novo protein synthesis.
Transcriptional activation of the human immunodeficiency virus type 1 long terminal repeat by hepatitis B virus X-protein requires de novo protein synthesis.
复制标题
乙型肝炎病毒 X 蛋白对人类免疫缺陷病毒 1 型长末端重复序列的转录激活需要从头合成蛋白质。
DOI：
10.1016/0042-6822(90)90501-h
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发表时间：
1990
期刊：
影响因子：
3.7
通讯作者：
Robinson,WS
中科院分区：
文献类型：
--
作者：
Twu,JS;Wu,JY;Robinson,WS
人B型肝炎病毒（HBV）X基因具有编码17-kDa多肽（命名为pX 17）的能力，以前已证明它能够反式激活人β-干扰素基因、人免疫缺陷病毒I型（HIV-1）长末端重复序列（LTR）、猿猴病毒40（SV 40）和HBV的异源调节元件。我们现在报告，pX 17在大肠杆菌中合成激活转录控制的HIV-1 LTR使用原生质体融合技术。E.将含有大肠杆菌的预合成X蛋白与淋巴细胞H938细胞融合，该细胞携带具有CAT基因的质粒的整合拷贝，该CAT基因在HIV-1 LTR（HIV-1 LTR CAT）的控制下，并且观察到CAT mRNA的稳态表达的显著增加。当用蛋白质合成抑制剂环己酰胺处理相同的融合细胞时，HIV-1 LTR的pX 17依赖性激活被消除。这一结果表明，X蛋白在E.大肠杆菌中的HBV X蛋白具有生物活性，提示在该系统中HBV X蛋白介导的HIV-1 LTR的反式激活需要新生细胞蛋白的合成。
Human hepatitis B virus (HBV) X-gene, previously shown to be capable oftrans-activating heterologous regulatory elements of the human β-interferon gene, the human immunodeficiency virus type I (HIV-1) long terminal repeat (LTR), the simian virus 40 (SV40), and HBV, has the capacity to code for a 17-kDa polypeptide (designated pX17). We now report that pX17synthesized inEscherichia colican activate transcription controlled by the HIV-1 LTR using a protoplast fusion technique. Protoplasts ofE. coli-containing presynthesized X-protein were fused with lymphocytic H938 cells harboring an integrated copy of a plasmid with the CAT gene under control of the HIV-1 LTR (HIV-1 LTR CAT) and a marked increase in the steady state expression of the CAT mRNA was observed. When the same fused cells were treated with the protein synthesis inhibitor cyclohexamide, the pX17-dependent activation of the HIV-1 LTR was abolished. This result indicates that the X-protein expressed inE. coliis biologically active and suggests that the HBV X-protein-mediatedtrans-activation of the HIV-1 LTR in this system requiresde novocellular protein synthesis.