Mori N, Prager D
Department of Medicine, Cedars-Sinai Medical Center, University of California-Los Angeles School of Medicine 90048, USA.
Cancer Res. 1996 Feb 15;56(4):779-82.
Human T-cell leukemia virus type I (HTLV-I) is the etiological agent for adult T-cell leukemia and tropical spastic paraparesis/HTLV-I-associated myelopathy. Recently, the transcription factor AP-2 has been demonstrated to be capable of activating gene expression from HTLV-I long terminal repeat. To determine whether changes occur in the levels of AP-2-binding activity in HTLV-I-infected cell lines, we compared the levels of AP-2 binding of nuclear extracts obtained from HTLV-I-infected T-cell lines with those of nuclear extracts obtained from uninfected T-cell lines. High levels of AP-2-binding activity were observed in HTLV-I-infected cell lines (MT-2, HUT-102, and SLB-1) using the mobility shift assay. In contrast, in the uninfected cell lines (Jurkat, HUT-78, and MLA 144), AP-2-binding activity was obviously low compared with that in the HTLV-I-infected cell lines. HTLV-I transactivator protein tax activates expression of both viral and cellular genes. We have demonstrated further that introduction of the tax gene into Jurkat cells stimulated AP-2-binding activity. These results indicate that HTLV-I-infected T cells exhibit constitutive AP-2-binding activity, and that tax may increase the DNA binding activity of AP-2.
人类嗜T淋巴细胞病毒I型（HTLV-I）是成人T细胞白血病和热带痉挛性截瘫/HTLV-I相关脊髓病的病原体。最近，转录因子AP-2已被证明能够激活HTLV-I长末端重复序列的基因表达。为了确定HTLV-I感染的细胞系中AP-2结合活性水平是否发生变化，我们比较了从HTLV-I感染的T细胞系获得的核提取物与从未感染的T细胞系获得的核提取物的AP-2结合水平。使用迁移率变动分析在HTLV-I感染的细胞系（MT-2、HUT-102和SLB-1）中观察到高水平的AP-2结合活性。相比之下，在未感染的细胞系（Jurkat、HUT-78和MLA 144）中，AP-2结合活性明显低于HTLV-I感染的细胞系。HTLV-I反式激活蛋白tax可激活病毒和细胞基因的表达。我们进一步证明，将tax基因导入Jurkat细胞可刺激AP-2结合活性。这些结果表明，HTLV-I感染的T细胞表现出组成性的AP-2结合活性，并且tax可能增加AP-2的DNA结合活性。
