Cellular transformation by the HTLV-I Tax protein, a jack-of-all-trades

Oncogene. 2003 Aug 11;22(33):5141-9. doi: 10.1038/sj.onc.1206549.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Aneuploidy
  • Animals
  • Cell Cycle
  • Cell Transformation, Neoplastic*
  • DNA Damage
  • DNA Repair
  • G1 Phase
  • G2 Phase
  • Gene Expression Regulation, Neoplastic*
  • Gene Expression Regulation, Viral
  • Gene Products, tax / metabolism
  • Gene Products, tax / physiology*
  • Humans
  • Leukemia, T-Cell / virology
  • Mitosis
  • Models, Biological
  • S Phase
  • Transcription, Genetic
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Gene Products, tax
  • Tumor Suppressor Protein p53