Diversion of stress granules and P-bodies during viral infection

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APOBEC3B drives PKR-mediated translation shutdown and protects stress granules in response to viral infection

Typical Stress Granule Proteins Interact with the 3′ Untranslated Region of Enterovirus D68 To Inhibit Viral Replication

Viruses, Free Full-Text

Viruses, Free Full-Text

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RIG-I and PKR, but not stress granules, mediate the pro-inflammatory response to Yellow fever virus

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CCR4, a RNA decay factor, is hijacked by a plant cytorhabdovirus phosphoprotein to facilitate virus replication

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Label-Free Quantitative Phosphoproteomic Analysis Reveals Differentially Regulated Proteins and Pathway in PRRSV-Infected Pulmonary Alveolar Macrophages

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APOBEC3B drives PKR-mediated translation shutdown and protects stress granules in response to viral infection

Stress granule formation, disassembly, and composition are regulated by alphavirus ADP-ribosylhydrolase activity

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