ArticleCell death & disease2019
G3BP1 inhibits RNA virus replication by positively regulating RIG-I-mediated cellular antiviral response.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
What it found
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Who cites it
77 citing papers in PubMed, 108 citations in OpenAlex.
- Unraveling the Multifaceted Role of TRIM21 in Virus-Triggered Innate Immunity and Diseases.Biomolecules · 2026Review
- NAP1 switches from an activator to a limiter of interferon induction by trapping TBK1 in condensates.Nature communications · 2026Article
- Alphavirus nsP3 as a multifunctional orchestrator of virus-host interplay.Journal of virology · 2026Review
- Article
- WFDC21P is essential for G3BP1-mediated RIG-I activation and antitumor immunity in triple-negative breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Dysregulated miRNAs and downstream gene expression associated with poor treatment response in first-episode psychosis.Brain, behavior, & immunity - health · 2026Article
- Cereblon induces G3BP2 neosubstrate degradation using molecular surface mimicry.Nature structural & molecular biology · 2026Article
- N6-methyladenosine within transmissible gastroenteritis virus genomic RNA inhibits its replication via efficient recognition by RNA sensor RIG-I.Journal of virology · 2026Article
- Key residues in SARS-CoV-2 NSP3 hypervariable region are necessary to modulate early stress granule activity.Journal of virology · 2026Article
- G3BP1 methylation by PRMT5 facilitates its recruitment of TBK1 for IRF3 activation during host response to foreign ribonucleic acids.Frontiers in immunology · 2026Article
- PRRSV GP2a blocks the RLR signaling pathway by targeting RIG-I.Journal of virology · 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
- Granular Insights on Innate and Intrinsic Immunity to Flaviviruses.Microorganisms · 2025Review
- The coronavirus 3CL protease: Unveiling its complex host interactions and central role in viral pathogenesis.Virologica Sinica · 2025Review
- Article
- Pseudorabies virus IE180 protein hijacks G3BPs into the nucleus to inhibit stress granule formation.Journal of virology · 2025Article
- Signalling by co-operative higher-order assembly formation: linking evidence at molecular and cellular levels.The Biochemical journal · 2025Review
- G3BP1 Regulates the Cell Cycle by Promoting IFNβ Production to Promote PCV2 Replication and Promotes Nuclear Transfer of Viral Proteins by Direct Binding.International journal of molecular sciences · 2025Article
- Regulation of viral replication by host restriction factors.Frontiers in immunology · 2025Review
- Drugs Targeting Sirtuin 2 Exhibit Broad-Spectrum Anti-Infective Activity.Pharmaceuticals (Basel, Switzerland) · 2024Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Retinoic acid-inducible gene I (RIG-I) is a pattern recognition receptor and is involved in the innate immune response against RNA viruses infection. Here, we demonstrate that the Ras-GTPase-activating protein SH3-domain-binding protein 1 (G3BP1) serves as a positive regulator of the RIG-I-mediated signaling pathway. G3BP1-deficient cells inhibited RNA virus-triggered induction of downstream antiviral genes. Furthermore, we found that G3BP1 inhibited the replication of Sendai virus and vesicular stomatitis virus, indicating a positive regulation of G3BP1 to cellular antiviral responses. Mechanistically, G3BP1 formed a complex with RNF125 and RIG-I, leading to decreased RNF125 via its auto-ubiquitination; thus, promoting expression of RIG-I. Overall, the results suggest a novel mechanism for G3BP1 in the positive regulation of antiviral signaling mediated by RIG-I.
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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.