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一种因子在体内与金属硫蛋白1基因启动子的金属反应元件的金属依赖性结合。

Metal-dependent binding of a factor in vivo to the metal-responsive elements of the metallothionein 1 gene promoter.

作者信息

Andersen R D, Taplitz S J, Wong S, Bristol G, Larkin B, Herschman H R

机构信息

Laboratory of Biomedical and Environmental Sciences, University of California at Los Angeles 90024.

出版信息

Mol Cell Biol. 1987 Oct;7(10):3574-81. doi: 10.1128/mcb.7.10.3574-3581.1987.

Abstract

Using the technique of genomic footprinting, we demonstrate cadmium-inducible protection from dimethyl sulfate (DMS) modification of guanine residues in vivo in five metal-responsive elements (MREs) in the promoter of the rat metallothionein 1 (MT-1) gene. We also identify a site of extreme DMS hyperreactivity which, like the MRE protection, occurs only after metal ion induction. With this hyperreactive site as an indicator, we can measure the kinetics of induction and deinduction. Changes in the intracellular metal ion concentrations are reflected in alterations in the reactivity with DMS of guanine residues in the MT-1 gene promoter. Lastly, for both control and metal-induced cells, we observe DMS protection and enhancement of a binding site (located 5' of the distal MRE) which is a consensus sequence for the Sp1 transcription factor. Transfection experiments with deletion mutations of a fusion gene construct indicate both that a sequence region which includes this GC box regulates the basal level of expression of the MT-1 gene and that increasing the number of MREs in the promoter increases the induced level of transcription. Our genomic footprinting and transfection data together suggest that (i) a transcription factor, possibly Sp1, plays an important role in regulating the basal level of expression of the MT-1 gene and (ii) metal induction involves the metal-dependent binding to a sequence-specific binding factor which responds to changes in intracellular metal ion levels.

摘要

利用基因组足迹技术,我们证明了在大鼠金属硫蛋白1(MT-1)基因启动子中的五个金属反应元件(MRE)中,镉可在体内诱导对鸟嘌呤残基的硫酸二甲酯(DMS)修饰产生保护作用。我们还确定了一个DMS超反应性极强的位点,该位点与MRE保护一样,仅在金属离子诱导后出现。以这个超反应性位点为指标,我们可以测量诱导和去诱导的动力学。细胞内金属离子浓度的变化反映在MT-1基因启动子中鸟嘌呤残基与DMS反应性的改变上。最后,对于对照细胞和金属诱导细胞,我们都观察到了一个结合位点(位于远端MRE的5'端)的DMS保护和增强,该位点是Sp1转录因子的共有序列。对融合基因构建体缺失突变进行的转染实验表明,包含该GC框的序列区域既调节MT-1基因的基础表达水平,又表明启动子中MRE数量的增加会提高诱导转录水平。我们的基因组足迹和转染数据共同表明:(i)一种转录因子,可能是Sp1,在调节MT-1基因的基础表达水平中起重要作用;(ii)金属诱导涉及金属依赖性结合到一个序列特异性结合因子上,该因子对细胞内金属离子水平的变化作出反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b11c/368011/66ac2410e549/molcellb00082-0216-a.jpg

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