ArticleJournal of innate immunity2017
Inducible GBP5 Mediates the Antiviral Response via Interferon-Related Pathways during Influenza A Virus Infection.
Article in Journal of innate immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
53 citing papers in PubMed, 71 citations in OpenAlex.
- Transcriptomic and proteomic signatures following AS03-adjuvanted Influenza A/H7N9 vaccine.Frontiers in immunology · 2026Trial
- Evaluation of the Xpert MTB Host Response assay for the triage of patients with presumed pulmonary tuberculosis: a prospective diagnostic accuracy study in Viet Nam, India, the Philippines, Uganda, and South Africa.The Lancet. Global health · 2024Trial
- Novel RT‒qPCR-based blood signatures for the diagnosis of pulmonary tuberculosis.Scientific reports · 2026Article
- Knockdown of GBP5 Attenuates Abdominal Aortic Aneurysm Formation via the NF-κB Pathway.Applied biochemistry and biotechnology · 2026Article
- Aberrant expression of GBP5 in tumor-infiltrating immune cells as an onco-immunological biomarker in pan-cancer.Discover oncology · 2026Article
- The Utility of a Three-gene Host Response to Discriminate Tuberculous Meningitis From Other Infections in Children.The Pediatric infectious disease journal · 2026Article
- Reactive oxygen species promotion drives auranofin's antiviral activity against hepatitis E virus.Journal of virology · 2026Article
- 3-Gene-TB-SCORE Accuracy for Tuberculosis Disease Diagnosis Is Not Affected by Immune-Mediated Inflammatory Disease Comorbidity.International journal of molecular sciences · 2025Article
- Review
- Guanylate-binding protein 5: a promising biomarker and therapeutic target.Infection and immunity · 2025Review
- Guanylate binding proteins (GBPs) as novel therapeutic targets against single-stranded RNA viruses.Molecular biology reports · 2025Review
- Role of guanylate-binding protein 5 in inflammatory diseases, immune diseases, cancers, and its potential therapeutic implications.Inflammopharmacology · 2025Review
- HTLV-1-infected cells drive the differentiation of monocytes into macrophages in vitro.BMC immunology · 2025Article
- Clinical significance and pathogenesis of GBP5 in infectious mononucleosis associated liver injury.Italian journal of pediatrics · 2025Article
- STAT1 mediates the pro-inflammatory role of GBP5 in colitis.Communications biology · 2025Article
- Guanylate-binding protein 5 antagonizes viral glycoproteins independently of furin processing.mBio · 2024Article
- The Furin Protease Dependence and Antiviral GBP2 Sensitivity of Murine Leukemia Virus Infection Are Determined by the Amino Acid Sequence at the Envelope Glycoprotein Cleavage Site.International journal of molecular sciences · 2024Article
- The Ability of a 3-Gene Host Signature in Blood to Distinguish Tuberculous Meningitis From Other Brain Infections.The Journal of infectious diseases · 2024Article
- The pseudogene GBP1P1 suppresses influenza A virus replication by acting as a protein decoy for DHX9.Journal of virology · 2024Article
- Diminished Immune Response and Elevated Abundance in Gut Microbe Dubosiella in Mouse Models of Chronic Colitis with GBP5 Deficiency.Biomolecules · 2024Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Guanylate binding protein (GBP) 5 belongs to the GBP family, which is involved in important cellular processes, including signal transduction, translation, vesicle trafficking, and exocytosis. Structurally, GBPs display a high degree of homology and share highly conserved GTP-binding or hydrolysis domains. GBP5 was reported to be a critical cellular factor in inflammasome assembly. However, little is known about its role in the host antiviral innate immune response. In this study, we found that GBP5 expression was significantly elevated in influenza patients and influenza A virus-infected A549 human lung epithelial cells. The overexpression of GBP5 inhibited virus replication by enhancing the expression of virus-induced interferon (IFN) and IFN-related effectors. Knockdown of GBP5 had the opposite effect. Moreover, GBP5 enhanced endogenous IFN expression by interacting with the NF-κB-essential modulator complex and stimulating NF-κB signaling. Additionally, the expression of proinflammatory factors, such as IL-6, IL-8, tumor necrosis factor-α, cyclooxygenase-2, and inducible nitric oxide synthase, was also activated by GBP5. Taken together, our results reveal that GBP5 inhibited virus replication through the activation of IFN signaling and proinflammatory factors.
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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.