ArticleJournal of virology2014
Herpes simplex virus 1 protein kinase US3 hyperphosphorylates p65/RelA and dampens NF-κB activation.
Article in Journal of virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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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.
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Who cites it
84 citing papers in PubMed, 112 citations in OpenAlex.
- Divergent Strategies in Innate Immune Evasion: A Comparative Review of Three Alphaherpesvirus Subfamily Members-PRV, HSV-1, and VZV.Transboundary and emerging diseases · 2026Review
- HSV-1 US3: A Master Mimic Hijacking Host Kinase Networks for Viral Dominance.Journal of medical virology · 2025Review
- Impact of the changes in substrate specificity of herpes simplex virus 1 protein kinase Us3 on viral infectionJournal of virology · 2025Article
- Macrophage WEE1 Directly Binds to and Phosphorylates NF-κB p65 Subunit to Induce Inflammatory Response and Drive Atherosclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- White spot syndrome virus immediate-early protein (wsv100) antagonizes the NF-κB pathway to inhibit innate immune response in shrimp.PLoS pathogens · 2025Article
- Marek's disease virus protein kinase US3 inhibits DNA-sensing antiviral innate immunity via abrogating activation of NF-κB.Microbiology spectrum · 2025Article
- HHV-6B ribonucleotide reductase sequesters NF-κB subunit p65 to inhibit innate immune responses.iScience · 2025Article
- The antiviral activity of myricetin against pseudorabies virus through regulation of the type I interferon signaling pathway.Journal of virology · 2025Article
- Article
- Identifying an Abnormal Phosphorylated Adaptor by Viral Kinase Using Mass Spectrometry.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Post-translational modifications as a key mechanism for herpes simplex virus type I evasion of host innate immunity.Frontiers in microbiology · 2025Review
- A Better Understanding of the Clinical and Pathological Changes in Viral Retinitis: Steps to Improve Visual Outcomes.Microorganisms · 2024Review
- GFPT2: A novel biomarker in mesothelioma for diagnosis and prognosis and its molecular mechanism in malignant progression.British journal of cancer · 2024Article
- Article
- Impaired endocytosis and accumulation in early endosomal compartments defines herpes simplex virus-mediated disruption of the nonclassical MHC class I-related molecule MR1.The Journal of biological chemistry · 2024Article
- DNA-PK and ATM drive phosphorylation signatures that antagonistically regulate cytokine responses to herpesvirus infection or DNA damage.Cell systems · 2024Article
- When ASFV Infection Meets the cGAS-STING Signaling Pathway.Transboundary and emerging diseases · 2024Review
- Several Alphaherpesviruses Interact Similarly with the NF-κB Pathway and Suppress NF-κB-Dependent Gene Expression.Microbiology spectrum · 2023Article
- Epstein-Barr Virus Envelope Glycoprotein gp110 Inhibits IKKi-Mediated Activation of NF-κB and Promotes the Degradation of β-Catenin.Microbiology spectrum · 2023Article
- Inhibitors of One or More Cellular Aurora Kinases Impair the Replication of Herpes Simplex Virus 1 and Other DNA and RNA Viruses with Diverse Genomes and Life Cycles.Microbiology spectrum · 2023Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear factor κB (NF-κB) plays important roles in innate immune responses by regulating the expression of a large number of target genes involved in the immune and inflammatory response, apoptosis, cell proliferation, differentiation, and survival. To survive in the host cells, viruses have evolved multiple strategies to evade and subvert the host immune response. Herpes simplex virus 1 (HSV-1) bears a large DNA genome, with the capacity to encode many different viral proteins to counteract the host immune responses. In the present study, we demonstrated that HSV-1 protein kinase US3 significantly inhibited NF-κB activation and decreased the expression of inflammatory chemokine interleukin-8 (IL-8). US3 was also shown to hyperphosphorylate p65 at serine 75 and block its nuclear translocation. Two US3 mutants, K220M and D305A, still interacted with p65; however, they could not hyperphosphorylate p65, indicating that the kinase activity of US3 was indispensable for the function. The attenuation of NF-κB activation by HSV-1 US3 protein kinase may represent a critical adaptation to enable virus persistence within the host. Importance: This study demonstrated that HSV-1 protein kinase US3 significantly inhibited NF-κB activation and decreased the expression of inflammatory chemokine interleukin-8 (IL-8). US3 hyperphosphorylated p65 at serine 75 to inhibit NF-κB activation. The kinase activity of US3 was indispensable for its hyperphosphorylation of p65 and abrogation of the nuclear translocation of p65. The present study elaborated a novel mechanism of HSV-1 US3 to evade the host innate immunity.
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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.