ArticleCell reports2024
Interaction between host G3BP and viral nucleocapsid protein regulates SARS-CoV-2 replication and pathogenicity.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 54 citations in OpenAlex.
- Surface Plasmon Resonance-Based Analysis of Ligand Binding Kinetics in Chikungunya Virus Drug Discovery.Methods in molecular biology (Clifton, N.J.) · 2027Article
- Loss-of-function mutation in Omicron variants reduces spike protein expression and attenuates SARS-CoV-2 infection.Nature communications · 2026Article
- Antagonism of stress granules key for SARS-CoV-2 infection and pathogenesis.bioRxiv : the preprint server for biology · 2026Article
- Alphaviral Capsid Proteins Inhibit Stress Granule Assembly via Competitive RNA Binding With G3BP1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Evolution of a truncated nucleocapsid protein enhances SARS-CoV-2 fitness by suppressing antiviral responses.PLoS biology · 2026Article
- Key residues in SARS-CoV-2 NSP3 hypervariable region are necessary to modulate early stress granule activity.Journal of virology · 2026Article
- Dissecting the Interaction Domains of SARS-CoV-2 Nucleocapsid Protein and Human RNA Helicase DDX3X and Search for Potential Inhibitors.International journal of molecular sciences · 2026Article
- Targeted stress granule regulation by engineering a non-catalytic O-GlcNAc transferase.Nature communications · 2026Article
- Pharmacological modulation of stress granulesFrontiers in pharmacology · 2026Review
- SARS-CoV-2 nsp14 induces the mCommunications biology · 2025Article
- SARS-CoV-2 and MERS-CoV disrupt host protein synthesis via nsp1 with differential effects on the integrated stress response.bioRxiv : the preprint server for biology · 2025Article
- 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
- The SARS-CoV-2 N protein disrupts G3BP1 function and alters lipid metabolism in COVID-19 pathogenesis.Archives of virology · 2025Article
- ASPL couples the assembly of stress granules with their VCP-mediated disassembly.Science advances · 2025Article
- SARS-CoV-2 Nsp15 endoribonuclease subverts host defenses to enhance viral fitness in lung cells.Journal of virology · 2025Article
- Granular Insights on Innate and Intrinsic Immunity to Flaviviruses.Microorganisms · 2025Review
- Spatial Transcriptomics and Single Cell-RNASeq Reveals Cellular Heterogeneity of SARS-CoV-2 in Lung Tissues and Global Mutational Patterns in COVID-19 Patients.Journal of medical virology · 2025Article
- Screening and identification of host factors interacting with the nucleocapsid protein of SARS-CoV-2 omicron variant using the yeast two-hybrid system.BMC microbiology · 2025Article
- The furin cleavage site is required for pathogenesis, but not transmission, of SARS-CoV-2.Journal of virology · 2025Article
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Authors and funding
28 authors at 3 institutions in 2 countries.
Funding
Abstract
G3BP1/2 are paralogous proteins that promote stress granule formation in response to cellular stresses, including viral infection. The nucleocapsid (N) protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) inhibits stress granule assembly and interacts with G3BP1/2 via an ITFG motif, including residue F17, in the N protein. Prior studies examining the impact of the G3PB1-N interaction on SARS-CoV-2 replication have produced inconsistent findings, and the role of this interaction in pathogenesis is unknown. Here, we use structural and biochemical analyses to define the residues required for G3BP1-N interaction and structure-guided mutagenesis to selectively disrupt this interaction. We find that N-F17A mutation causes highly specific loss of interaction with G3BP1/2. SARS-CoV-2 N-F17A fails to inhibit stress granule assembly in cells, has decreased viral replication, and causes decreased pathology in vivo. Further mechanistic studies indicate that the N-F17-mediated G3BP1-N interaction promotes infection by limiting sequestration of viral genomic RNA (gRNA) into stress granules.
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