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  • Title: High levels of AP-2-binding activity in cell lines infected with human T-cell leukemia virus type I: possible enhancement of AP-2 binding by human T-cell leukemia virus type I tax.
    Author: Mori N, Prager D.
    Journal: Cancer Res; 1996 Feb 15; 56(4):779-82. PubMed ID: 8631013.
    Abstract:
    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.
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