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衰老过程中,小鼠大脑中USF1/USF2与α-Pal/Nrf1对Fmr-1启动子的相互作用增强。

Interaction of USF1/USF2 and alpha-Pal/Nrf1 to Fmr-1 promoter increases in mouse brain during aging.

作者信息

Prasad S, Singh Kanchan

机构信息

Biochemistry & Molecular Biology Lab, CAS in Zoology, Banaras Hindu University, Varanasi, Uttar Pradesh 221005, India.

出版信息

Biochem Biophys Res Commun. 2008 Nov 14;376(2):347-51. doi: 10.1016/j.bbrc.2008.08.155. Epub 2008 Sep 7.

Abstract

Fragile X syndrome is caused due to silencing of FMR-1 gene transcription leading to loss of fragile X mental retardation protein (FMRP). To investigate whether the transcriptional mechanism is linked to aging, we have studied interaction of the transcription factors USF1/USF2 and alpha-Pal/Nrf1 to E-box and GC-box, respectively, in Fmr-1 promoter in the brain of young, adult, and old mouse using electrophoretic mobility shift assay (EMSA). Our data reveal that the interaction of these transcription factors to their respective promoter sequences increases in mouse brain as a function of age. The finding on the interaction of the above transcription factors to their cognate sequences is novel as the current investigation has been carried out in intact and aging mouse. The present finding is important in respect to age- and FMRP-dependent brain function.

摘要

脆性X综合征是由于FMR-1基因转录沉默导致脆性X智力低下蛋白(FMRP)缺失所致。为了研究转录机制是否与衰老有关,我们使用电泳迁移率变动分析(EMSA)研究了转录因子USF1/USF2和α-Pal/Nrf1分别与幼年、成年和老年小鼠大脑中Fmr-1启动子的E-box和GC-box的相互作用。我们的数据显示,这些转录因子与其各自启动子序列的相互作用在小鼠大脑中随年龄增长而增加。上述转录因子与其同源序列相互作用的这一发现是新颖的,因为目前的研究是在完整和衰老的小鼠中进行的。就年龄和FMRP依赖的脑功能而言,目前的发现很重要。

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