首页> 外文OA文献 >The ATF/CREB transcription factor-binding site in the polymerase beta promoter mediates the positive effect of N-methyl-N'-nitro-N-nitrosoguanidine on transcription.
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The ATF/CREB transcription factor-binding site in the polymerase beta promoter mediates the positive effect of N-methyl-N'-nitro-N-nitrosoguanidine on transcription.

机译:聚合酶β启动子中的ATF / CREB转录因子结合位点介导N-甲基-N'-硝基-N-亚硝基胍对转录的积极影响。

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摘要

DNA polymerase beta (pol beta) is a constitutively expressed DNA repair enzyme in vertebrate cells. Yet, it had been shown previously that the pol beta mRNA level increases in Chinese hamster ovary (CHO) cells within 4 h after treatment with several monofunctional DNA damaging agents, notably, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). Herein we report that a transfected pol beta promoter fusion gene is activated by MNNG treatment of CHO cells; mRNA from the transfected gene is approximately 10-fold higher in treated cells than in untreated cells 16 h after treatment. This activation is mediated through the decanucleotide palindromic element GTGACGTCAC at positions -49 to -40 in the "TATA-less" core promoter. This element, which is similar to the ATF/CREB transcription factor-binding site in a number of mammalian genes, forms the center of a strong protein-binding site for CHO cell nuclear extract proteins. Mutated pol beta promoter fusion genes lacking the element fail to bind protein at this site and fail to respond to MNNG treatment of cells.
机译:DNA聚合酶beta(pol beta)是脊椎动物细胞中组成型表达的DNA修复酶。但是,以前已经证明,在用几种单功能DNA破坏剂(尤其是N-甲基-N'-硝基-N-亚硝基胍(MNNG))处理后的4小时内,中国仓鼠卵巢(CHO)细胞中polβmRNA水平升高)。在本文中,我们报道了通过MNNG处理CHO细胞激活了转染的polβ启动子融合基因;处理后16小时,在处理过的细胞中,来自转染基因的mRNA比未处理的细胞高约10倍。该活化通过“少TATA”核心启动子中第-49至-40位的十核苷酸回文元件GTGACGTCAC介导。该元素与许多哺乳动物基因中的ATF / CREB转录因子结合位点相似,形成了CHO细胞核提取蛋白的强蛋白结合位点的中心。缺少该元素的突变pol beta启动子融合基因无法在该位点结合蛋白质,并且无法响应MNNG处理细胞。

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