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TR3孤儿受体对人睫状神经营养因子受体(CNTFRα)基因内含子增强子的诱导作用。

Induction of an intronic enhancer of the human ciliary neurotrophic factor receptor (CNTFRalpha) gene by the TR3 orphan receptor.

作者信息

Mu X M, Young W J, Liu Y X, Uemura H, Chang C

机构信息

Department of Pathology, University of Rochester, NY 14642, USA.

出版信息

Endocrine. 1998 Aug;9(1):27-32. doi: 10.1385/ENDO:9:1:27.

Abstract

A hormone response element, CNTFRalpha-NBRE (5'-AAAGGTCA-3') has been identified in the fifth intron of the alpha component of ciliary neurotrophic factor receptor gene (CNTFR-15) for the human TR3 orphan receptor (TR3). A specific binding between in vitro expressed TR3 and CNTFRalpha-NBRE was demonstrated by using electrophoretic mobility shift assay. A reporter gene assay using chloramphenicol acetyl-transferase (CAT) showed that CNTFR-15 has an enhancer activity that could be induced by TR3 in a dose-dependent manner. This induction was significantly reduced in the absence of CNTFRalpha-NBRE. Together, these results indicate CNTFRalpha-NBRE is sufficient to mediate TR3 action in inducing the enhancer activity of CNTFR-15. Our finding may, therefore, suggest CNTFRalpha is a target gene regulated by TR3 and expand the role of TR3 in the nervous system.

摘要

在人TR3孤儿受体(TR3)的睫状神经营养因子受体基因(CNTFR - 15)α组分的第五个内含子中,已鉴定出一种激素反应元件CNTFRα - NBRE(5'-AAAGGTCA-3')。通过电泳迁移率变动分析证明了体外表达的TR3与CNTFRα - NBRE之间存在特异性结合。使用氯霉素乙酰转移酶(CAT)的报告基因分析表明,CNTFR - 15具有增强子活性,该活性可被TR3以剂量依赖性方式诱导。在不存在CNTFRα - NBRE的情况下,这种诱导作用显著降低。总之,这些结果表明CNTFRα - NBRE足以介导TR3诱导CNTFR - 15增强子活性的作用。因此,我们的发现可能提示CNTFRα是受TR3调控的靶基因,并扩展了TR3在神经系统中的作用。

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