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首页> 外文期刊>Molecular and Cellular Biology >β-Catenin Upregulates the Constitutive and Virus-Induced Transcriptional Capacity of the Interferon Beta Promoter through T-Cell Factor Binding Sites
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β-Catenin Upregulates the Constitutive and Virus-Induced Transcriptional Capacity of the Interferon Beta Promoter through T-Cell Factor Binding Sites

机译：β-Catenin通过T细胞因子结合位点上调干扰素Beta启动子的组成型和病毒诱导的转录能力

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Rapid upregulation of interferon beta (IFN-β) expression following virus infection is essential to set up an efficient innate antiviral response. Biological roles related to the antiviral and immune response have also been associated with the constitutive production of IFN-β in naive cells. However, the mechanisms capable of modulating constitutive IFN-β expression in the absence of infection remain largely unknown. In this work, we demonstrate that inhibition of the kinase glycogen synthase kinase 3 (GSK-3) leads to the upregulation of the constitutive level of IFN-β expression in noninfected cells, provided that GSK-3 inhibition is correlated with the binding of β-catenin to the IFN-β promoter. Under these conditions, IFN-β expression occurred through the T-cell factor (TCF) binding sites present on the IFN-β promoter independently of interferon regulatory factor 3 (IRF3). Enhancement of the constitutive level of IFN-β per se was able to confer an efficient antiviral state to naive cells and acted in synergy with virus infection to stimulate virus-induced IFN-β expression. Further emphasizing the role of β-catenin in the innate antiviral response, we show here that highly pathogenic Rift Valley fever virus (RVFV) targets the Wnt/β-catenin pathway and the formation of active TCF/β-catenin complexes at the transcriptional and protein level in RVFV-infected cells and mice.
机译：病毒感染后干扰素β（IFN-β）表达的快速上调对于建立有效的先天抗病毒反应至关重要。与抗病毒和免疫反应有关的生物学作用还与幼稚细胞中IFN-β的组​​成型产生有关。然而，在没有感染的情况下，能够调节组成型IFN-β表达的机制仍然未知。在这项工作中，我们证明了抑制激酶糖原合酶激酶3（GSK-3）会导致非感染细胞中IFN-β表达的组成型水平上调，但前提是GSK-3抑制与β的结合相关-catenin与IFN-β启动子结合。在这些条件下，IFN-β的表达通过IFN-β启动子上的T细胞因子（TCF）结合位点发生，而与干扰素调节因子3（IRF3）无关。 IFN-β本身的组成水平的增强能够赋予幼稚细胞有效的抗病毒状态，并与病毒感染协同作用以刺激病毒诱导的IFN-β表达。进一步强调了β-catenin在先天抗病毒反应中的作用，我们在这里表明，高致病性的裂谷热病毒（RVFV）靶向Wnt /β-catenin途径，并在转录和转录过程中形成活性TCF /β-catenin复合物。 RVFV感染的细胞和小鼠中的蛋白质水平。

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