Li X H, Gaynor R B
Division of Hematology-Oncology, Department of Medicine, Harold Simmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1583-90. doi: 10.1089/08892220050192994.
The Tax protein encoded by the human T cell leukemia virus type I virus (HTLV-1) activates the expression of both viral genes and cellular genes involved in T lymphocyte growth and proliferation. One of the critical cellular pathways activated by Tax is NF-kappaB. NF-kappaB is normally sequestered in the cytoplasm, bound to a family of inhibitory proteins known as I-kappaB. In contrast to the transient activation of the NF-kappaB pathway seen in response to cytokines, Tax results in constitutive nuclear levels of NF-kappaB. Tax activation of the NF-kappaB pathway is mediated by its ability to enhance the phosphorylation and subsequent degradation of I-kappaB. The persistent activation of the NF-kappaB pathway by Tax is believed to be one of the major events involved in HTLV-1-mediated cellular transformation of T lymphocytes. This review summarizes data exploring the role of Tax in activating the NF-kappaB pathway and discusses our studies to determine the mechanism by which Tax activates the NF-kappaB pathway.
人类I型T细胞白血病病毒（HTLV-1）编码的Tax蛋白可激活病毒基因以及参与T淋巴细胞生长和增殖的细胞基因的表达。Tax激活的关键细胞途径之一是核因子κB（NF-κB）。NF-κB通常被隔离在细胞质中，与一类称为I-κB的抑制蛋白结合。与细胞因子刺激后NF-κB途径的短暂激活不同，Tax可导致NF-κB持续存在于细胞核中。Tax对NF-κB途径的激活是通过增强I-κB的磷酸化及随后的降解来介导的。Tax对NF-κB途径的持续激活被认为是HTLV-1介导的T淋巴细胞细胞转化的主要事件之一。本综述总结了探索Tax在激活NF-κB途径中作用的数据，并讨论了我们为确定Tax激活NF-κB途径的机制所开展的研究。
