不同的病毒诱导增强元件之间的转录协同作用机制
1Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, Massachusetts 02138.
Cell
|September 10, 1993
概括
高流动性组蛋白HMG I(Y) 对于干扰素β基因调节至关重要. 它通过促进转录因子NF-kappa B和激活转录因子2 (ATF-2) 之间的相互作用来增强病毒诱导元素PRDII和PRDIV的活性.
科学领域:
- 分子生物学分子生物学
- 基因规则 基因规则
- 免疫学 免疫学 免疫学
背景情况:
- 人类干扰素β基因促进体含有可诱导病毒的调节元素.
- 积极的调节域II (PRDII) 活动需要高流动性组蛋白HMG I(Y) 和转录因子NF-kappa B.
研究的目的:
- 调查HMG I(Y) 在PRDIV活动中的作用,这是与PRDII协同作用的监管要素.
- 阐明HMG I(Y) 对转录协同作用的分子机制.
主要方法:
- 电泳运动转移试验 (EMSA) 用于研究蛋白质-DNA相互作用.
- 同免疫沉试验用于分析蛋白质与蛋白质相互作用.
- 对响应病毒诱导的调节元件活性进行分析.
主要成果:
- HMG I(Y) 对于PRDIV活动至关重要,与PRDII协同工作.
- HMG I(Y) 促进了激活转录因子2 (ATF-2) 的结合以及含有ATF-2和c-Jun. 的可诱导复合物的组合.
- HMG I(Y) 与ATF-2的氨酸拉链/基础区域直接相互作用,ATF-2与NF-kappa B.相互作用.
结论:
- HMG I(Y) 在建立PRDII和PRDIV之间的转录协同作用方面发挥着关键的结构性作用.
- HMG I(Y) 促进NF-kappa B和ATF-2之间的相互作用,从而促进它们的活动和/或约束.
- 这种机制对于干扰素β基因的病毒诱导表达至关重要.
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