Bex F, Gaynor R B
Departments of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, 75235-8594, USA.
Methods. 1998 Sep;16(1):83-94. doi: 10.1006/meth.1998.0646.
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 IL-2 receptor genes via increases in nuclear levels of NF-kappaB. Tax modulation of gene expression via the ATF/CREB and NF-kappaB pathways is linked to its transforming properties. This review discusses the mechanisms by which Tax regulates viral and cellular gene expression.
人类嗜T淋巴细胞病毒I型(HTLV-I)是成人T细胞白血病的病原体。HTLV-I编码的一种蛋白质Tax可激活病毒基因表达,并且对于转化T淋巴细胞至关重要。Tax通过与ATF/CREB蛋白以及共激活因子CBP/p300相互作用来激活HTLV-I基因表达,这些蛋白会在HTLV-I长末端重复序列(LTR)中被称为21碱基对重复序列的调控元件上组装成多蛋白复合物。Tax还可通过提高核内NF-κB水平来激活包括白细胞介素-2(IL-2)和IL-2受体基因在内的细胞基因的表达。Tax通过ATF/CREB和NF-κB途径对基因表达的调节与其转化特性相关。本综述讨论了Tax调节病毒和细胞基因表达的机制。