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SUMOylation of p53 mediates interferon activities

机译：p53的SUMOylation介导干扰素活性

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There is growing evidence that many host proteins involved in innate and intrinsic immunity are regulated by SUMOylation, and that SUMO contributes to the regulatory process that governs the initiation of the type I interferon (IFN) response. The tumor suppressor p53 is a modulator of the IFN response that plays a role in virus-induced apoptosis and in IFN-induced senescence. Here we demonstrate that IFN treatment increases the levels of SUMOylated p53 and induces cellular senescence through a process that is partially dependent upon SUMOylation of p53. Similarly, we show that vesicular stomatitis virus (VSV) infection induces p53 SUMOylation, and that this modification favors the control of VSV replication. Thus, our study provides evidence that IFN signaling induces p53 SUMOylation, which results in the activation of a cellular senescence program and contributes to the antiviral functions of interferon.
机译：越来越多的证据表明，许多参与先天性和内在免疫力的宿主蛋白都受到SUMOylation的调节，而SUMO参与了控制I型干扰素（IFN）应答启动的调节过程。肿瘤抑制因子p53是IFN反应的调节剂，在病毒诱导的凋亡和IFN诱导的衰老中起作用。在这里，我们证明了IFN处理可提高SUMO酰化p53的水平，并通过部分依赖p53的SUMOylation的过程诱导细胞衰老。同样，我们显示水泡性口炎病毒（VSV）感染诱导p53 SUMOylation，并且此修改有利于控制VSV复制。因此，我们的研究提供了证据，证明IFN信号传导可诱导p53 SUMOylation，从而激活细胞衰老程序，并有助于干扰素的抗病毒功能。

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