Catching BETs by viruses.

Catching BETs by viruses.
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DOI:
10.1016/j.bbagrm.2022.194859
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发表时间:
2022-10
期刊:
Biochimica et biophysica acta. Gene regulatory mechanisms
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其他
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病毒利用多种手段劫持宿主细胞机制,逃避先天免疫反应,维持自身生命周期。作为关键的转录调节因子,人类BET蛋白是越来越多病毒的重要靶标。BET蛋白通过其溴结构域与乙酰化组蛋白的相互作用与染色质结合,而这些蛋白的羧基末端结构域包含各种人类共转录调节因子的对接位点。然而,同样的对接位点可以被病毒蛋白占据,这些病毒蛋白利用BET蛋白将其基因组成分锚定在受感染宿主细胞的染色质上。在这篇综述中,我们重点介绍了BET蛋白在病毒感染时的病理功能,重点讨论了它们与病毒蛋白(如SARS-CoV-2的包膜蛋白)直接相互作用的机制。
Viruses use diverse tactics to hijack host cellular machineries to evade innate immune responses and maintain their life cycles. Being critical transcriptional regulators, human BET proteins are prominent targets of a growing number of viruses. The BET proteins associate with chromatin through the interaction of their bromodomains with acetylated histones, whereas the carboxy-terminal domains of these proteins contain docking sites for various human co-transcriptional regulators. The same docking sites however can be occupied by viral proteins that exploit the BET proteins to anchor their genome components to chromatin in the infected host cell. In this review we highlight the pathological functions of the BET proteins upon viral infection, focusing on the mechanisms underlying their direct interactions with viral proteins, such as the envelope protein from SARS-CoV-2.
选择性抑制BET溴结构域。
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