ArticleVirus research2018
The canonical Wnt/β-catenin signaling pathway stimulates herpes simplex virus 1 productive infection.
Article in Virus research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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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
22 citing papers in PubMed, 38 citations in OpenAlex.
- Downregulation of the host ribonucleotide reductase subunit M2 via the Wnt/β-catenin pathway is a novel mechanism for duck plague virus replication and a potential antiviral target.Poultry science · 2026Article
- Multi-proteomic profiling of the varicella-zoster virus-host interface reveals host susceptibilities to severe infection.Nature microbiology · 2025Article
- PGK1 enhances productive bovine herpesvirus 1 infection by stimulating β-catenin-dependent transcription.Veterinary research · 2025Article
- Aryl hydrocarbon receptor facilitates HSV-1 lytic infection by enhancing viral gene transcription and receptor expression.Frontiers in cellular and infection microbiology · 2025Article
- Viral Factors in Modulation of Host Immune Response: A Route to Novel Antiviral Agents and New Therapeutic Approaches.International journal of molecular sciences · 2024Review
- The heterogeneous sensitivity of pediatric brain tumors to different oncolytic viruses is predicted by unique gene expression profiles.Molecular therapy. Oncology · 2024Article
- Nuclear envelope budding: Getting large macromolecular complexes out of the nucleus.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024Article
- Analysis of miRNAs involved in mouse brain injury upon Coxsackievirus A6 infection.Frontiers in cellular and infection microbiology · 2024Article
- Wnt3a Facilitates SARS-CoV-2 Pseudovirus Entry into Cells.International journal of molecular sciences · 2023Article
- Centralspindlin proteins Pavarotti and Tumbleweed along with WASH regulate nuclear envelope budding.The Journal of cell biology · 2023Article
- Host factors associated with either VP16 or VP16-induced complex differentially affect HSV-1 lytic infection.Reviews in medical virology · 2022Review
- The complex relationship between integrins and oncolytic herpes Simplex Virus 1 in high-grade glioma therapeutics.Molecular therapy oncolytics · 2022Review
- Involvement of the Wnt pathway in BVDV cytopathogenic strain replication in primary bovine cells.Virology journal · 2022Article
- Regulation of herpes simplex virus type 1 latency-reactivation cycle and ocular disease by cellular signaling pathways.Experimental eye research · 2022Article
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- Wnt antagonists suppress herpes simplex virus type 1 productive infection.Antiviral research · 2021Article
- Disruption of innate defense responses by endoglycosidase HPSE promotes cell survival.JCI insight · 2021Article
- Integrative analysis of microRNA and mRNA expression profiles in MARC-145 cells infected with PRRSV.Virus genes · 2020Article
- β-cantenin is potentially involved in the regulation of c-Jun signaling following bovine herpesvirus 1 infection.Veterinary microbiology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
The ability of herpes simplex virus 1 (HSV-1) to replicate efficiently in differentiated cells is regulated by cellular factors that stimulate viral gene expression, cell survival, and viral morphogenesis. Activation of the canonical Wnt signaling pathway generally increases β-catenin protein levels, cell survival, and growth in dividing cells suggesting this important signaling pathway regulates productive infection. In this study, we demonstrated that a β-catenin specific small molecule inhibitor (iCRT14) reduced HSV-1 titers approximately 10-fold in primary human lung fibroblasts and Vero cells. Furthermore, β-catenin dependent transcription was increased at late times after infection and as expected iCRT14 reduced β-catenin dependent transcription. Although HSV-1 infection increased β-catenin steady state protein levels approximately 4-fold in Vero cells, there was only a nominal increase in human lung fibroblasts. We hypothesized that VP16 regulates β-catenin dependent transcription because VP16 is a viral regulatory protein expressed at late times after infection. In the absence of other viral proteins, VP16 increased β-catenin dependent transcription and β-catenin steady state protein levels. Collectively, these studies suggested the cellular transcription factor β-catenin stimulates productive infection, in part because VP16 enhances β-catenin dependent transcription.
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What OpenQuestion holds
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.