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Catching BETs by viruses

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 i...

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Bibliographic Details
Published in:Biochimica et biophysica acta. Gene regulatory mechanisms 2022-10, Vol.1865 (7), p.194859-194859, Article 194859
Main Authors: Zandian, Mohamad, Chen, Irene P., Byrareddy, Siddappa N., Fujimori, Danica Galonić, Ott, Melanie, Kutateladze, Tatiana G.
Format: Article
Language:English
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Summary: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. •Human BET transcriptional coactivators are targets of several viral proteins.•Herpesvirus episome integrates into host chromatin via binding to BRD4-ET.•Acetylated SARS-CoV-2 E protein binds to bromodomains of BRD2/4.•BRD4-CTD is recognized by proteins from human and bovine papillomaviruses.
ISSN:1874-9399
1876-4320
1876-4320
DOI:10.1016/j.bbagrm.2022.194859