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首页> 外文期刊>Molecular and Cellular Biology >Interferon regulatory factors and TFIIB cooperatively regulate interferon-responsive promoter activity in vivo and in vitro.
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Interferon regulatory factors and TFIIB cooperatively regulate interferon-responsive promoter activity in vivo and in vitro.

机译：干扰素调节因子和TFIIB在体内和体外协同调节干扰素应答性启动子活性。

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Interferon regulatory factors (IRFs) bind to the interferon-stimulated response element (ISRE) and regulate interferon- and virus-mediated gene expression. IRF-1 acts as a transcriptional activator, while IRF-2 acts as a repressor. Here we show that IRF-1 and IRF-2 bind to both cellular TFIIB, a component of the basal transcription machinery, and recombinant TFIIB (rTFIIB) and that this protein-protein interaction facilitates binding of IRFs to the ISRE. A functional interaction between TFIIB and IRF was assessed by a newly established in vitro transcription assay in which recombinant IRF-1 (rIRF-1) stimulated transcription specifically from an ISRE-containing template. With this assay we show that rIRF-1 and rTFIIB cooperatively enhance the ISRE promoter in vitro. We found that the activity of an ISRE-containing promoter was cooperatively enhanced upon cotransfection of TFIIB and IRF-1 cDNAs into P19 embryonal carcinoma cells, further demonstrating functional interactions in vivo. The cooperative enhancement by TFIIB and IRF-1 was independent of the TATA sequence in the ISRE promoter but dependent on the initiator sequence (Inr) and was abolished when P19 cells were induced to differentiate by retinoic acid treatment. In contrast, cotransfection of TFIIB and IRF-1 into NIH 3T3 cells resulted in a dose-dependent repression of promoter activation which occurred in a TATA-dependent manner. Our results indicate the presence of a cell type-specific factor that mediates the functional interaction between IRFs and TFIIB and that acts in conjunction with the requirement of TATA and Inr for promoter activation.
机译：干扰素调节因子（IRF）与干扰素刺激的反应元件（ISRE）结合并调节干扰素和病毒介导的基因表达。 IRF-1充当转录激活因子，而IRF-2充当阻遏因子。在这里，我们显示IRF-1和IRF-2与细胞TFIIB（基础转录机制的一个组成部分）和重组TFIIB（rTFIIB）都结合，并且这种蛋白质相互作用促进了IRF与ISRE的结合。通过新建立的体外转录测定法评估了TFIIB和IRF之间的功能相互作用，其中重组IRF-1（rIRF-1）特异性地刺激了含有ISRE的模板的转录。通过该测定，我们表明rIRF-1和rTFIIB在体外协同增强ISRE启动子。我们发现，将TFIIB和IRF-1 cDNA共转染到P19胚胎癌细胞中后，含ISRE启动子的活性得到协同增强，进一步证明了体内的功能相互作用。 TFIIB和IRF-1的协同增强作用独立于ISRE启动子中的TATA序列，但取决于引发剂序列（Inr），并且在视黄酸处理诱导P19细胞分化时被取消。相反，将TFIIB和IRF-1共转染到NIH 3T3细胞中会导致启动子激活的剂量依赖性抑制，该抑制以TATA依赖性方式发生。我们的结果表明，存在介导IRF和TFIIB之间功能相互作用的细胞类型特异性因子，并与启动子激活所需的TATA和Inr共同起作用。

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