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Manipulation of ubiquitin/SUMO pathways in human herpesviruses infection

机译:操纵人类疱疹病毒感染中的泛素/ SUMO途径

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摘要

Post-translational modification of proteins with ubiquitin/small ubiquitin-like modifier (SUMO) molecules triggers multiple signaling pathways that are critical for many aspects of cellular physiology. Given that viruses hijack the biosynthetic and degradative systems of their host, it is not surprising that viruses encode proteins to manipulate the host's cellular machinery for ubiquitin/SUMO modification at multiple levels. Infection with a herpesvirus, among the most ubiquitous human DNA viruses, has been linked to many human diseases, including cancers. The interplay between human herpesviruses and the ubiquitylation/SUMOylation modification system has been extensively investigated in the past decade. In this review, we present an overview of recent advances to address how the ubiquitin/SUMO-modified system alters the latency and lytic replication of herpesvirus and how herpesviruses usurp the ubiquitin/SUMO pathways against the host's intrinsic and innate immune response to favor their pathogenesis.
机译:用泛素/小泛素样修饰剂(SUMO)分子对蛋白质进行翻译后修饰会触发多种信号通路,这些通路对于细胞生理学的许多方面都是至关重要的。鉴于病毒劫持了其宿主的生物合成和降解系统,因此,病毒编码蛋白质以操纵宿主的细胞机制以进行多种泛素/ SUMO修饰就不足为奇了。在最普遍的人类DNA病毒中,疱疹病毒的感染与许多人类疾病(包括癌症)有关。在过去的十年中,人类疱疹病毒和泛素化/ SUMOylation修饰系统之间的相互作用已得到广泛研究。在本综述中,我们概述了最近的进展,以解决遍在蛋白/ SUMO修饰的系统如何改变疱疹病毒的潜伏期和裂解复制以及疱疹病毒如何侵害遍在蛋白/ SUMO途径抵抗宿主的内在和先天免疫应答以促进其发病机理。

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