Cellular transformation by the HTLV-I Tax protein, a jack-of-all-trades.
The human T-cell leukemia virus type I (HTLV-I) is an oncogenic retrovirus that is responsible for adult T-cell leukemia and a neurological disease, HTLV-I-associated myelopathy/tropical spastic paraparesis. HTLV-I encodes an oncogenic protein, Tax, which affects a variety of cellular functions prompting it to be referred to as a jack-of-all trades. The ability of Tax to both transcriptionally regulate cellular gene expression and to functionally inactivate proteins involved in cell-cycle progression and DNA repair provide the basis for Tax-mediated transformation and leukemogenesis. This review will concentrate on the effects of Tax on the dysregulation of the G(1)/S and G(2)/M checkpoints as well as the suppression of DNA damage repair leading to cellular transformation.
Gatza
Michael L
ML
Interdepartmental Program in Cell and Molecular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Watt
Julie C
JC
Marriott
Susan J
SJ
D000782:Aneuploidy; D000818:Animals; D002453:Cell Cycle; D002471:Cell Transformation, Neoplastic; D004249:DNA Damage; D004260:DNA Repair; D016193:G1 Phase; D016195:G2 Phase; D015972:Gene Expression Regulation, Neoplastic; D015967:Gene Expression Regulation, Viral; D016356:Gene Products, tax / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D015458:Leukemia, T-Cell / Q000821:virology; D008938:Mitosis; D008954:Models, Biological; D016196:S Phase; D014158:Transcription, Genetic; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
D016356:Gene Products, tax; D016159:Tumor Suppressor Protein p53