@article{oai:niigata-u.repo.nii.ac.jp:00006345,
 author = {MORI, Naoki and YAMAMOTO, Naoki and FUJII, Masahiro},
 issue = {3},
 journal = {Acta medica et biologica, Acta medica et biologica},
 month = {Sep},
 note = {Human T-Cell leukemia virus type I (HTLV-I) is a human retrovirus that is associated with the development of adult T-cell leukemia (ATL) and HTLV-I-associated myelopathy/tropical spastic paraparesis. The 40 kDa viral protein Tax is thought to play a critical role in the development of these diseases since it transforms human T lymphocytes in vitro, and induces various types of tumors in transgenic animals carrying tax gene. Tax was originally identified as the transcriptional activator of its own viral promoter in a long terminal repeat. Thereafter, Tax has been shown to dysregulate cellular growth control mechanisms by affecting the transcription of cellular genes. Tax does not bind directly to DNA, but instead interacts with cellular factors to modulate their activities. Host transcription factors whose activity is modulated by Tax include nuclear factor (NF)-κB/Rel. NF-κB/Rel transcription factors participate in the activation of numerous genes involved in immune regulation/inflammation as well as cellular growth control including genes encoding cytokines, cell surface receptors, adhesion molecules, and acute phase proteins. This article reviews the molecular mechanisms of Tax that affect NF-κB/Rel activity and the role of NF-κB/Rel in the regulation of celular genes expression as well as cellular transformation by HTLV-I. In addition, we present a possible alternative mechanism involved in the Tax-independent activation of NF-κB/Rel in ATL cells in vivo, which might be involved in the late stages of leukemogenesis.},
 pages = {85--96},
 title = {Activation of Nuclear Factor-B/Rel Proteins by Human T-Cell Leukemia Virus Type I},
 volume = {47},
 year = {1999}
}