Hoyos B, Ballard D W, Böhnlein E, Siekevitz M, Greene W C
Mount Sinai Medical Center, Department of Microbiology, New York, NY 10029.
Science. 1989 Apr 28;244(4903):457-60. doi: 10.1126/science.2497518.
Transcriptional activation of the human interleukin-2 (IL-2) gene, like induction of the IL-2 receptor alpha (IL-2R alpha) gene and the type 1 human immunodeficiency virus (HIV-1), is shown to be modulated by a kappa B-like enhancer element. Mutation of a kappa B core sequence identified in the IL-2 promoter (-206 to -195) partially inhibits both mitogen- and HTLV-I Tax-mediated activation of this transcription unit and blocks the specific binding of two inducible cellular factors. These kappa B-specific proteins (80 to 90 and 50 to 55 kilodaltons) similarly interact with the functional kappa B enhancer present in the IL-2R alpha promoter. These data suggest that these kappa B-specific proteins have a role in the coordinate regulation of this growth factor-growth factor receptor gene system that controls T cell proliferation.
人白细胞介素2（IL-2）基因的转录激活，如同IL-2受体α（IL-2Rα）基因和1型人类免疫缺陷病毒（HIV-1）的诱导一样，显示受κB样增强子元件调控。在IL-2启动子（-206至-195）中鉴定出的κB核心序列的突变部分抑制了丝裂原和HTLV-I Tax介导的该转录单元的激活，并阻断了两种可诱导细胞因子的特异性结合。这些κB特异性蛋白（80至90千道尔顿和50至55千道尔顿）同样与IL-2Rα启动子中存在的功能性κB增强子相互作用。这些数据表明，这些κB特异性蛋白在控制T细胞增殖的该生长因子-生长因子受体基因系统的协同调节中起作用。
