Transcription Factor Redundancy Ensures Induction of the Antiviral State
Transcription Factor Redundancy Ensures Induction of the Antiviral State
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DOI：
10.1074/jbc.m110.165936
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发表时间：
2010-12-31
影响因子：
4.8
通讯作者：
tenOever, Benjamin R.
中科院分区：
文献类型：
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作者：
Schmid, Sonja;Mordstein, Markus;tenOever, Benjamin R.
人们认为对病毒感染的转录反应主要是由干扰素（IFN）信号传导诱导的。在这里，我们证明，在没有 IFN 信号传导的情况下，仍然维持类似 IFN 的转录组。这种转录活性由 IFN 刺激反应元件 (ISRE) 介导，ISRE 与 IFN 刺激基因因子 3 (ISGF3) 以及 IFN 反应因子 7 (IRF7) 结合。通过结合体外生物化学和体内转录分析，我们剖析了 IRF 特异性、ISGF3 特异性或通用 ISRE 的构成。总而言之，这里提供的数据表明，IRF7 可以在缺乏 I 型或 III 型信号传导的情况下诱导 IFN 样转录组，因此为细胞提供一定程度的冗余，以确保诱导抗病毒状态。
The transcriptional response to virus infection is thought to be predominantly induced by interferon (IFN) signaling. Here we demonstrate that, in the absence of IFN signaling, an IFN-like transcriptome is still maintained. This transcriptional activity is mediated from IFN-stimulated response elements (ISREs) that bind to both the IFN-stimulated gene factor 3 (ISGF3) as well as to IFN response factor 7 (IRF7). Through a combination of both in vitro biochemistry and in vivo transcriptional profiling, we have dissected what constitutes IRF-specific, ISGF3-specific, or universal ISREs. Taken together, the data presented here suggest that IRF7 can induce an IFN-like transcriptome in the absence of type-I or -III signaling and therefore provides a level of redundancy to cells to ensure the induction of the antiviral state.