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首页> 外文期刊>Molecular and Cellular Biology >Positive and negative modulation of Jun action by thyroid hormone receptor at a unique AP1 site.
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Positive and negative modulation of Jun action by thyroid hormone receptor at a unique AP1 site.

机译：甲状腺激素受体在一个独特的AP1位点对Jun行为的正负调节。

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摘要

We have characterized the putative AP1 site in the backbone of pUC plasmids and found unique regulatory effects. The site, which mapped to a 19-bp region around nucleotide 37, conferred transcriptional activation by Jun or Jun/Fos that was boosted up to fivefold by unliganded thyroid hormone receptor (TR). Thyroid hormone changed potentiation of the Jun response by TR into repression. Although the plasmid sequence is a near-perfect consensus AP1 site, the perfect consensus AP1 site from the human collagenase promoter did not show the same effects. Deletion of the ligand binding domain of the TR eliminated the ability of the receptor to boost Jun activity, and deletion, mutation, or changes in specificity of the DNA binding domain eliminated both its ability to potentiate Jun activity and repress with hormone. In vitro Jun/Fos complexes bound the operative plasmid fragment, and the presence of TR interfered very little with Jun/Fos binding activity. Protein interaction studies in the absence of DNA showed that TR bound Jun protein in solution either in the presence or in the absence of hormone. These observations suggest a mechanism for synergy and repression by TR through modulation of Jun activity: positive when TR is unliganded, and negative when hormone is bound. They also suggest that the presence of the plasmid element can confound studies of the regulation of linked promoters.
机译：我们已经表征了pUC质粒的骨架中假定的AP1位点，并发现了独特的调节作用。该位点定位在核苷酸37周围的19 bp区域，被Jun或Jun / Fos赋予转录激活作用，而该作用被未结合的甲状腺激素受体（TR）增强了五倍。甲状腺激素将TR的Jun应答增强作用转变为抑制作用。尽管质粒序列是接近完美的共有AP1位点，但是来自人胶原酶启动子的完美共有AP1位点没有显示相同的作用。 TR的配体结合结构域的缺失消除了受体增强Jun活性的能力，并且DNA结合结构域的缺失，突变或特异性的变化消除了其增强Jun活性和抑制激素的能力。体外Jun / Fos复合物结合了有效的质粒片段，TR的存在对Jun / Fos结合活性的影响很小。在不存在DNA的情况下进行的蛋白质相互作用研究表明，在存在或不存在激素的情况下，TR均与溶液中的Jun蛋白结合。这些观察结果表明通过调节Jun活性来通过TR产生协同作用和抑制的机制：当TR未配体时为正，而结合激素时为负。他们还暗示，质粒元件的存在会混淆对连接的启动子调控的研究。

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