Functional characterization of interferon regulatory factor 3a (IRF-3a), an alternative splice isoform of IRF-3
Functional characterization of interferon regulatory factor 3a (IRF-3a), an alternative splice isoform of IRF-3
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DOI：
10.1128/mcb.21.13.4169-4176.2001
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发表时间：
2001-07-01
影响因子：
5.3
通讯作者：
Howley, PM
中科院分区：
文献类型：
--
作者：
Karpova, AY;Ronco, LV;Howley, PM
许多细胞类型的病毒感染导致病毒和干扰素（IFN）刺激基因的转录诱导。β IFN（IFN-β）基因是这些快速诱导的基因之一;它作为细胞防御反应的基本组成部分，引发有效的抗病毒，免疫调节和抗增殖作用。参与病毒感染后IFN-β产生的严格调节的转录因子之一是干扰素调节因子（IRF）3（IRF 3）。我们已经表征了IRF 3的选择性剪接同种型，我们称之为IRF-3a。IRF-3a可以选择性地和有效地抑制病毒诱导的IFN-β启动子的激活。IRF-3a缺乏IRF-3中发现的DNA结合结构域的一半，并且不能结合经典的IRF结合元件，即IFN刺激的应答元件。这些研究表明IRF-3a可能作为IRF 3的调节剂。
Virus infection of numerous cell types results in the transcriptional induction of a subset of virus- and interferon (IFN)-stimulated genes. The beta IFN (IFN-beta) gene is one of these rapidly induced genes; it serves as a fundamental component of the cellular defense response in eliciting potent antiviral, immunomodulatory, and antiproliferative effects. One of the transcription factors involved in the stringent regulation of IFN-beta production following virus infection is interferon regulatory factor (IRF) 3 (IRF3). We have characterized an alternatively spliced isoform of IRF3 that we have called IRF-3a. IRF-3a can selectively and potently inhibit virus-induced activation of the IFN-beta promoter. IRF-3a lacks half of the DNA binding domain found in IRF-3 and is unable to bind to the classical IRF binding elements, IFN-stimulated response elements. These studies suggest that IRF-3a may act as a modulator of IRF3.