HIV-1反式激活因子Tat促进RelB转录激活功能及机制初探  

Preliminary Study on Mechanism of HIV-1 Transactivator Tat Enhancing Transcription Activation of RelB

作　　者：王蒙 杨炜[1] 胡笑梅 陈宇 谈娟[1] 乔文涛[1] Wang Meng;Yang Wei;Hu Xiaomei;Chen Yu;Wang Jian;Tan Juan(Key laboratory of Molecular Microbiology and Biotechnology, Ministry of Education, College of Life Sciences, Nankai University, Tianjin 300071, China)

机构地区：[1]南开大学生命科学学院,分子微生物与技术教育部重点实验室,天津300071

出　　处：《南开大学学报（自然科学版）》2018年第6期41-47,共7页Acta Scientiarum Naturalium Universitatis Nankaiensis

基　　金：国家自然科学基金(81571988,31670151).

摘　　要：人免疫缺陷病毒I型(Human immunodeficiency virus type 1, HIV-1)是艾滋病的病原体.Tat是其编码的反式激活因子.为深入解析Tat在转录激活过程中的作用,在实验室前期发现Tat与RelB具有相互作用的基础上,确证了Tat可以促进RelB激活NF-κB;发现Tat促使细胞核内RelB增多;初步机制分析发现Tat不能促进细胞内p100的磷酸化和剪切,但可促进RelB乙酰化、磷酸化修饰.这些结果表明Tat可能通过改变RelB翻译后修饰增强RelB的转录激活活性.HIV Tat enables robust transcription from HIV-1 LTR and is able to modify the expression of cellular genes. In order to further understand the role of Tat in transcriptional activation, previously, we found that Tat and RelB interact with each other. In this study, we found that Tat could induce the accumulation of RelB in nuclear and enhance the activation of NF-κB pathway mediated by RelB. Preliminary mechanism analysis showed that Tat could strengthen the acetylation and phosphorylation of RelB, but not disturb the phosphorylation and processing of p100. Those results indicate that Tat could enhance the transcriptional activation of RelB through posttranslational modification.

关 键 词：NF-ΚB TAT RELB 转录激活 

分 类 号：R373[医药卫生—病原生物学]