| First Author | Ratner L | Year | 2000 |
| Journal | AIDS Res Hum Retroviruses | Volume | 16 |
| Issue | 16 | Pages | 1647-51 |
| PubMed ID | 11080805 | Mgi Jnum | J:66198 |
| Mgi Id | MGI:1928119 | Doi | 10.1089/08892220050193092 |
| Citation | Ratner L, et al. (2000) Studies of the immortalizing activity of HTLV type 1 tax, using an infectious molecular clone and transgenic mice. AIDS Res Hum Retroviruses 16(16):1647-51 |
| abstractText | Expression of Tax in the mature lymphoid compartment of transgenic mice resulted in a lymphoproliferative malignancy of natural killer cells and cytotoxic T lymphocytes. Transgenic mouse tumors exhibited mutations in the p53 tumor suppressor gene, and functional inactivation of wild-type p53 protein. Tax transgenic mice heterozygous for the p53 gene exhibited more rapid tumor dissemination and accelerated mortality. Studies of Tax trans-activation in an infectious clone of HTLV-1 demonstrated a critical role for nuclear factor B activation in lymphocyte immortalization. A mutant disrupting Tax activation of the cAMP response element binding (CREB) protein resulted in preferential immortalization of CD8(+) lymphocytes, rather than preferential immortalization of CD4(+) lymphocytes seen with the wild-type infectious clone. A mutation disrupting Tax interaction with CREB-binding protein, CBP, did not affect lymphocyte immortalization by the infectious molecular clone. These models provide new insights into the molecular details of HTLV-1 leukemogenesis. |
