摘要
Human T-cell leukemia virus type 1(HTLV-1),the first human retrovirus discovered,is the etiological agent of adult-T-cell leukemia/lymphoma.The HTLV-1 encoded Tax protein is a potent oncoprotein that deregulates gene expression by constitutively activating nuclear factor-κB(NF-κB).Tax activation of NF-κB is critical for the immortalization and survival of HTLV-1-infected T cells.In this review,we summarize the present knowledge on mechanisms underlying Tax-mediated NF-κB activation,with an emphasis on post-translational modifications of Tax.
Human T-cell leukemia virus type 1 (HTLV-1), the first human retrovirus discovered, is the etiological agent of adult-T-cell leukemia/lymphoma. The HTLV-1 encoded Tax protein is a potent oncoprotein that deregulates gene expression by constitutively activating nuclear factor-κ B (NF-κ B). Tax activation of NF-κ B is critical for the immortalization and survival of HTLV-1-infected T cells. In this review, we summarize the present knowledge on mechanisms underlying Tax-mediated NF-κ B activation, with an emphasis on post-translational modifications of Tax.
基金
Supported by Grants from the United States Public Health Service/National Institutes of Health,No.RO1CA135362,RO1GM083143 and PO1CA128115
