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 G1/S and Gz/M checkpoints as well as the suppression of DNA damage repair leading to cellular transformation.
Original language | English (US) |
---|---|
Pages (from-to) | 5141-5149 |
Number of pages | 9 |
Journal | Oncogene |
Volume | 22 |
Issue number | 33 REV. ISS. 2 |
DOIs | |
State | Published - Aug 11 2003 |
Externally published | Yes |
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Genetics
- Cancer Research
Keywords
- Cell cycle
- Cellular transformation
- DNA repair
- HTLV-I
- Tax