par Bex, Françoise 
;Gaynor, Richard
Référence Methods, 16, 1, page (83-94)
Publication Publié, 1998-09
;Gaynor, RichardRéférence Methods, 16, 1, page (83-94)
Publication Publié, 1998-09
Article révisé par les pairs
| Résumé : | The human T-cell leukemia virus type I or HTLV-I is the causative agent of adult T-cell leukemia. A protein encoded by HTLV-I, Tax, activates viral gene expression and is essential for transforming T-lymphocytes. Tax activates HTLV-I gene expression via interactions with the ATF/CREB proteins and the coactivators CBP/p300 which assemble as a multiprotein complex on regulatory elements known as 21-bp repeats in the HTLV-I LTR. Tax can also activate expression from cellular genes including the interleukin-2 (IL-2) and the L-2 receptor genes via increases in nuclear levels of NF-κB. Tax modulation of gene expression via the ATF/CREB and NF-κB pathways is linked to its transforming properties. This review discusses the mechanisms by which tax regulates viral and cellular gene expression. |
