ArticleViruses2020
Pseudorabies Virus UL24 Abrogates Tumor Necrosis Factor Alpha-Induced NF-κB Activation by Degrading P65.
Article in Viruses, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
27 citing papers in PubMed, 39 citations in OpenAlex.
- A Humanized Anti-gD Broadly Neutralizing Antibody Confers Complete Post-Exposure Protection Against Pseudorabies Virus.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Divergent Strategies in Innate Immune Evasion: A Comparative Review of Three Alphaherpesvirus Subfamily Members-PRV, HSV-1, and VZV.Transboundary and emerging diseases · 2026Review
- A glycoprotein D-targeted lipid nanoparticle-encapsulated mRNA vaccine elicits strong protective immunity against pseudorabies virus.Journal of virology · 2025Article
- Pseudorabies virus DNA polymerase processivity factor pUL42 inhibits type I IFN production by negatively regulating cGAS-STING signaling pathway.Journal of virology · 2025Article
- Recombinant pseudorabies virus expressing the consensus VP2 protein of porcine parvovirus 1 (PPV1) protects pigs against pseudorabies virus and PPV1.Veterinary research · 2025Article
- Alphaherpesvirus in Pets and Livestock.Microorganisms · 2025Review
- Commentary: Development and immunogenicity evaluation of a quadruple-gene-deleted pseudorabies virus strain.Frontiers in microbiology · 2025Article
- Evasion of the Antiviral Innate Immunity by PRV.International journal of molecular sciences · 2024Review
- Comparative Review of the Conserved UL24 Protein Family in Herpesviruses.International journal of molecular sciences · 2024Review
- KSHV ORF20 Promotes Coordinated Lytic Reactivation for Increased Infectious Particle Production.Viruses · 2024Article
- Development of an interpretable machine learning model associated with genetic indicators to identify Yin-deficiency constitution.Chinese medicine · 2024Article
- Pseudorabies virus UL38 attenuates the cGAS-STING signaling pathway by recruiting Tollip to promote STING for autophagy degradation.Virology journal · 2024Article
- TheFrontiers in veterinary science · 2024Article
- Development and immunogenicity evaluation of a quadruple-gene-deleted pseudorabies virus strain.Frontiers in microbiology · 2024Article
- Apoptosis is mediated by FeHV-1 through the intrinsic pathway and interacts with the autophagic process.Virology journal · 2023Article
- Progress on innate immune evasion and live attenuated vaccine of pseudorabies virus.Frontiers in microbiology · 2023Review
- Mechanism of herpesvirus UL24 protein regulating viral immune escape and virulence.Frontiers in microbiology · 2023Review
- Genome editing of pseudorabies virus in the CRISPR/Cas9 era: a mini-review.Frontiers in veterinary science · 2023Review
- Pseudorabies Virus ICP0 Abolishes Tumor Necrosis Factor Alpha-Induced NF-κB Activation by Degrading P65.Viruses · 2022Article
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor NF-κB plays a critical role in diverse biological processes. The NF-κB pathway can be activated by incoming pathogens and then stimulates both innate and adaptive immunity. However, many viruses have evolved corresponding strategies to balance NF-κB activation to benefit their replication. Pseudorabies virus (PRV) is an economically important pathogen that belongs to the alphaherpesvirus group. There is little information about PRV infection and NF-κB regulation. This study demonstrates for the first time that the UL24 protein could abrogate tumor necrosis factor alpha (TNF-α)-mediated NF-κB activation. An overexpression assay indicated that UL24 inhibits this pathway at or downstream of P65. Furthermore, co-immunoprecipitation analysis demonstrated that UL24 selectively interacts with P65. We demonstrated that UL24 could significantly degrade P65 by the proteasome pathway. For the first time, PRV UL24 was shown to play an important role in NF-κB evasion during PRV infection. This study expands our understanding that PRV can utilize its encoded protein UL24 to evade NF-κB signaling.
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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 Socratic graph.