ArticleCell discovery2021
SARS-CoV-2 nucleocapsid protein impairs stress granule formation to promote viral replication.
Article in Cell discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
What it found
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Who cites it
85 citing papers in PubMed, 122 citations in OpenAlex.
- Porcine deltacoronavirus nucleocapsid protein inhibits RIG-I signaling pathway by suppressing G3BP1-mediated stress granules formation.Virulence · 2026Article
- SARS-CoV-2 nucleocapsid induces hyperinflammation and vascular leakage through the Toll-like receptor signaling axis in macrophages.Science advances · 2026Article
- Stress granules formed during infections with RNA viruses have significant virus-specific differences in generation and composition.PLoS biology · 2026Article
- Assembly of lipid droplet-associated ring structures in hepatitis C virus-infected cells via liquid-liquid phase separation (LLPS) and non-LLPS mechanisms.Journal of virology · 2026Article
- Visualization of G3BP1-RNA Condensate Nascent Assembly and Early Maturation by HS-AFM.International journal of molecular sciences · 2026Article
- Differential assembly of RNP granules via activation of distinct dsRNA sensors by adenovirus mutants.PLoS pathogens · 2026Article
- Antagonism of stress granules key for SARS-CoV-2 infection and pathogenesis.bioRxiv : the preprint server for biology · 2026Article
- Evolution of a truncated nucleocapsid protein enhances SARS-CoV-2 fitness by suppressing antiviral responses.PLoS biology · 2026Article
- Review
- Alphaviral Capsid Proteins Inhibit Stress Granule Assembly via Competitive RNA Binding With G3BP1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Differential assembly of RNP granules via activation of distinct dsRNA sensors by adenovirus mutants.bioRxiv : the preprint server for biology · 2026Article
- Key residues in SARS-CoV-2 NSP3 hypervariable region are necessary to modulate early stress granule activity.Journal of virology · 2026Article
- Targeting biomolecular condensates: beyond dissolution.BMC biology · 2026Review
- Key residues in SARS-CoV-2 NSP3 hyper variable region are necessary to modulate early stress granule activity.bioRxiv : the preprint server for biology · 2025Article
- Analysis of the Porcine Reproductive and Respiratory Syndrome Virus Nucleocapsid Interactome.Journal of proteome research · 2025Article
- Human Coronavirus-229E Hijacks Key Host-Cell RNA-Processing Complexes for Replication.Journal of proteome research · 2025Article
- SARS-CoV-2 Nsp15 endoribonuclease subverts host defenses to enhance viral fitness in lung cells.Journal of virology · 2025Article
- Article
- Review
- Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The newly emerging coronavirus SARS-CoV-2 causes severe lung disease and substantial mortality. How the virus evades host defense for efficient replication is not fully understood. In this report, we found that the SARS-CoV-2 nucleocapsid protein (NP) impaired stress granule (SG) formation induced by viral RNA. SARS-CoV-2 NP associated with the protein kinase PKR after dsRNA stimulation. SARS-CoV-2 NP did not affect dsRNA-induced PKR oligomerization, but impaired dsRNA-induced PKR phosphorylation (a hallmark of its activation) as well as SG formation. SARS-CoV-2 NP also targeted the SG-nucleating protein G3BP1 and impaired G3BP1-mediated SG formation. Deficiency of PKR or G3BP1 impaired dsRNA-triggered SG formation and increased SARS-CoV-2 replication. The NP of SARS-CoV also targeted both PKR and G3BP1 to impair dsRNA-induced SG formation, whereas the NP of MERS-CoV targeted PKR, but not G3BP1 for the impairment. Our findings suggest that SARS-CoV-2 NP promotes viral replication by impairing formation of antiviral SGs, and reveal a conserved mechanism on evasion of host antiviral responses by highly pathogenic human betacoronaviruses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.