Inhibition of PKR by Viruses.
Inhibition of PKR by Viruses.
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DOI：
10.3389/fmicb.2021.757238
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发表时间：
2021
影响因子：
5.2
通讯作者：
Michiels T
中科院分区：
文献类型：
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作者：
Cesaro T;Michiels T
细胞通过检测非自身分子的传感器和效应器对病毒感染做出反应，效应器可以具有直接的抗病毒活动或调整细胞生理来限制病毒感染和传播。真核细胞翻译起始因子2α激酶2，更为人所知的是PKR，在对病毒感染的反应中既是传感器又是效应器。在感受到感染细胞中的双链RNA分子后，PKR自我激活，并主要通过阻断翻译机制和诱导细胞凋亡来发挥其抗病毒功能。病毒开发了许多策略来对抗PKR途径，从而强调了PKR的抗病毒效力。在这篇综述中，我们介绍了这类策略的多样性，从阻止PKR激活上游的双链RNA识别，到激活PKR靶标下游的eIF2B。
Cells respond to viral infections through sensors that detect non-self-molecules, and through effectors, which can have direct antiviral activities or adapt cell physiology to limit viral infection and propagation. Eukaryotic translation initiation factor 2 alpha kinase 2, better known as PKR, acts as both a sensor and an effector in the response to viral infections. After sensing double-stranded RNA molecules in infected cells, PKR self-activates and majorly exerts its antiviral function by blocking the translation machinery and inducing apoptosis. The antiviral potency of PKR is emphasized by the number of strategies developed by viruses to antagonize the PKR pathway. In this review, we present an update on the diversity of such strategies, which range from preventing double-stranded RNA recognition upstream from PKR activation, to activating eIF2B downstream from PKR targets.
影响因子：
--
作者：
Sudha G;Yamunadevi S;Tyagi N;Das S;Srinivasan N
通讯作者：
Srinivasan N