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甲状腺激素反应元件的新定位与功能

Novel location and function of a thyroid hormone response element.

作者信息

Bigler J, Eisenman R N

机构信息

Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98104, USA.

出版信息

EMBO J. 1995 Nov 15;14(22):5710-23. doi: 10.1002/j.1460-2075.1995.tb00258.x.

DOI:10.1002/j.1460-2075.1995.tb00258.x
PMID:8521828
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC394686/
Abstract

We describe a novel thyroid hormone response element (TRE)-containing sequence, clone 144, isolated by immunoprecipitation of nuclear thyroid hormone receptor (TR)-DNA complexes from the rat pituitary tumor cell line GH4. These cells express several mRNAs of approximately 10 kb that hybridize to the TRE-containing genomic clone 144. These mRNAs are up-regulated at the transcriptional level in the absence of thyroid hormone (T3) and repressed in its presence. The sequence protected from DNase I digestion by TR in clone 144 contains two consensus TRE half-sites arranged as inverted palindromes. The clone 144 TRE is located in the 3' untranslated region (UTR) of several related mRNAs. A reporter construct transfected into 293 cells was responsive to TR regulation when the clone 144 TRE was inserted in the 3' UTR but not when inserted upstream of the promoter. As found for the endogenous 144 mRNAs, the 144 TRE reporter construct is activated by TR in the absence of T3, but not in its presence. Deletion analysis showed that clone 144 sequences flanking the TRE were necessary for TR-mediated regulation, suggesting that the mechanism by which TR regulates transcription through a TRE in the 3' UTR is different from that through the TREs located in the promoter region.

摘要

我们描述了一个含有新型甲状腺激素反应元件（TRE）的序列，即克隆144，它是通过对大鼠垂体肿瘤细胞系GH4的核甲状腺激素受体（TR）-DNA复合物进行免疫沉淀分离得到的。这些细胞表达几种约10 kb的mRNA，它们与含有TRE的基因组克隆144杂交。这些mRNA在无甲状腺激素（T3）时在转录水平上调，而在有T3时受到抑制。克隆144中受TR保护不被DNase I消化的序列包含两个作为反向回文排列的共有TRE半位点。克隆144 TRE位于几种相关mRNA的3'非翻译区（UTR）。当克隆144 TRE插入到293细胞转染的报告基因构建体的3' UTR中时，该构建体对TR调节有反应，而插入到启动子上游时则无反应。正如对内源144 mRNA所发现的那样，144 TRE报告基因构建体在无T3时被TR激活，而在有T3时则不被激活。缺失分析表明，TRE侧翼的克隆144序列对于TR介导的调节是必需的，这表明TR通过3' UTR中的TRE调节转录的机制与通过启动子区域中的TRE调节转录的机制不同。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/9f03f27c6ca5/emboj00046-0273-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/7f3b691de8c2/emboj00046-0265-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/ef0ec61cc02b/emboj00046-0266-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/1cef9d8087e1/emboj00046-0267-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/5aeb90d6aa90/emboj00046-0268-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/17eab023ec23/emboj00046-0269-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/65a8a6ffbdd6/emboj00046-0270-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/20a650928c36/emboj00046-0271-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/58f70f92797f/emboj00046-0272-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/9f03f27c6ca5/emboj00046-0273-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/7f3b691de8c2/emboj00046-0265-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/ef0ec61cc02b/emboj00046-0266-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/1cef9d8087e1/emboj00046-0267-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/5aeb90d6aa90/emboj00046-0268-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/17eab023ec23/emboj00046-0269-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/65a8a6ffbdd6/emboj00046-0270-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/20a650928c36/emboj00046-0271-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/58f70f92797f/emboj00046-0272-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7655/394686/9f03f27c6ca5/emboj00046-0273-a.jpg

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