辅助抑制因子SMRT特异性抑制孤儿核受体hB1F/hLRH-1的转录活性。

Ping-Long Xu, Yu-Ying Kong, You-Hua Xie, Yuan Wang
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引用次数: 0

摘要

孤儿核受体hB1F(也称为NR5A2、LRH-1、FTF或CPF)在调节多种细胞和病毒基因的表达中发挥重要作用,这些基因积极参与胆酸生物合成、肝脏特异性基因调控网络和乙型肝炎病毒复制等广泛的生物学过程。核受体的活性受多种机制调控,包括共激活和共抑制。在这项研究中,我们发现维甲酸受体和甲状腺激素受体(SMRT)的沉默介质特异性地抑制hB1F的转录活性,无论是在GAL4依赖性报告系统上还是在hB1F应答的HBV增强子II/核心启动子上。在不同的细胞系中观察到SMRT施加的抑制作用。有趣的是,hB1F不能直接与SMRT相互作用,正如哺乳动物双杂交分析或GST下拉实验所证明的那样。综上所述,我们首次得出结论,hB1F的转录活性是由辅助抑制因子SMRT通过一种间接机制特异性调节的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Corepressor SMRT specifically represses the transcriptional activity of orphan nuclear receptor hB1F/hLRH-1.

The orphan nuclear receptor hB1F (also known as NR5A2, LRH-1, FTF or CPF) plays important roles in regulating the expression of several cellular and viral genes actively involved in a wide range of biological processes such as the bile acid biosynthesis, liver specific gene regulatory network and hepatitis B virus replication. The activity of nuclear receptors is regulated by multiple mechanisms, including coactivation and corepression. In this study, it was found that the silencing mediator for retinoic acid receptor and thyroid hormone receptor (SMRT) specifically represses the transcriptional activity of hB1F, on either GAL4 dependent reporter system or the hB1F-responsive HBV enhancer II/core promoter. The repression imposed by SMRT is observed in different cell lines. Interestingly, hB1F couldn t interact with SMRT directly, as demonstrated by mammalian two-hybrid analysis or GST pull-down assay. Taken together, it can be concluded for the first time that the transcriptional activity of hB1F is regulated specifically by the corepressor SMRT via an indirect mechanism.

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