Constitutive expression of the HTLV-I pX and env regions in Jurkat T-cells induces differential activation of SRE, CRE and NF kappa B pathways.
Constitutive expression of the HTLV-I pX and env regions in Jurkat T-cells induces differential activation of SRE, CRE and NF kappa B pathways.
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Jurkat T细胞中HTLV-1 pX和env区域的组成型表达诱导SRE、CRE和NF kappa B途径的差异激活。
DOI：
10.1023/a:1007906823269
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发表时间：
1997
期刊：
影响因子：
1.6
通讯作者：
Tabibzadeh,S
中科院分区：
文献类型：
--
作者：
Black,AC;Luo,J;Chun,S;Tabibzadeh,S
人类T细胞白血病病毒I型（HTLV-I）导致成人T细胞白血病/淋巴瘤（ATLL）。HTLV Tax是一种病毒转录激活因子，可以激活多种细胞基因。然而，HTLV介导的T细胞转化可能涉及从单剪接以及双剪接的病毒mRNA表达的另外的病毒蛋白。为了确定这些病毒蛋白对Jurkat T细胞中细胞基因表达的组合作用，我们获得了组成型表达HTLV-I pX和env区的稳定转染子（J3.9）。通过北方印迹，J3.9细胞显示出显著增加的CD 25和GM-CSF的mRNA水平，但没有诱导CD 25或GM-CSF。这种模式对应于在瞬时基因表达测定中激活的是一个EST-I，而不是一个GM-CSF启动子驱动的报告基因构建体。在DNA电泳迁移率变动分析（EMSA）中，与J-Neo细胞提取物相比，J3.9细胞的核提取物与CRE和SRE的结合显著增加，但与核因子κ B（NFκB）DNA寡核苷酸的结合没有增加。这些结果表明，Jurkat T细胞中pX和env区基因产物的低水平表达刺激CRE和SRE诱导的细胞基因的持续活化，但不刺激NFκ B诱导的细胞基因的持续活化。
Human T-cell leukemia virus type I (HTLV-I) causes adult T-cell leukemia/lymphoma (ATLL). HTLV Tax, the viral transcriptional activator, can activate a variety of cellular genes. HTLV-mediated T-cell transformation, however, may involve additional viral proteins expressed from singly- as well as doubly-spliced viral mRNA. To determine the combined effect of these viral proteins on cellular gene expression in Jurkat T-cells, we derived stable transfectants that constitutively express the HTLV-I pX and env regions (J3.9). J3.9 cells show substantially increased mRNA levels of egr-1 and c-jun but no induction of either CD25 or GM-CSF by Northern blotting. This pattern corresponded to the activation of an egr-1 but not a GM-CSF promoter-driven reporter construct in transient gene expression assays. In DNA electrophoretic mobility shift assays (EMSA), nuclear extract from J3.9 cells has significantly increased binding to CRE and SRE but not nuclear factor kappa B (NFκB) DNA oligos, as compared to J-Neo cell extract. These results suggest that low level expression of pX and env region gene products in Jurkat T-cells stimulates persistent activation of CRE- and SRE- but not NFκB-induced cellular genes.