ArticleJournal of virology2007
Varicella-zoster virus infection of human fibroblast cells activates the c-Jun N-terminal kinase pathway.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 45 citations in OpenAlex.
- Varicella Zoster Virus Neuronal Latency and Reactivation Modeled in Vitro.Current topics in microbiology and immunology · 2023Review
- Receptors for Respiratory Syncytial Virus Infection and Host Factors Regulating the Life Cycle of Respiratory Syncytial Virus.Frontiers in cellular and infection microbiology · 2022Review
- The Roles of c-Jun N-Terminal Kinase (JNK) in Infectious Diseases.International journal of molecular sciences · 2021Review
- Targeting Host Cellular Factors as a Strategy of Therapeutic Intervention for Herpesvirus Infections.Frontiers in cellular and infection microbiology · 2021Review
- Antiviral Activities of Quercetin and Isoquercitrin Against Human Herpesviruses.Molecules (Basel, Switzerland) · 2020Article
- Modeling Varicella Zoster Virus Persistence and Reactivation - Closer to Resolving a Perplexing Persistent State.Frontiers in microbiology · 2019Review
- Role of the JNK Pathway in Varicella-Zoster Virus Lytic Infection and Reactivation.Journal of virology · 2017Article
- Article
- BX-795 inhibits HSV-1 and HSV-2 replication by blocking the JNK/p38 pathways without interfering with PDK1 activity in host cells.Acta pharmacologica Sinica · 2017Article
- JNK1 Derived from Orange-Spotted Grouper, Epinephelus coioides, Involving in the Evasion and Infection of Singapore Grouper Iridovirus (SGIV).Frontiers in microbiology · 2016Article
- Study of vaccinia and cowpox viruses' replication in Rac1-N17 dominant-negative cells.Memorias do Instituto Oswaldo Cruz · 2013Article
- Potential of protein kinase inhibitors for treating herpesvirus-associated disease.Trends in microbiology · 2013Review
- Amplification of JNK signaling is necessary to complete the murine gammaherpesvirus 68 lytic replication cycle.Journal of virology · 2012Article
- Posttranslational modification of vesicular stomatitis virus glycoprotein, but not JNK inhibition, is the antiviral mechanism of SP600125.Journal of virology · 2012Article
- Varicella-Zoster virus ORF12 protein triggers phosphorylation of ERK1/2 and inhibits apoptosis.Journal of virology · 2012Article
- SP600125 inhibits Orthopoxviruses replication in a JNK1/2 -independent manner: Implication as a potential antipoxviral.Antiviral research · 2012Article
- JNK1 is required for lentivirus entry and gene transfer.Journal of virology · 2011Article
- Compounds that target host cell proteins prevent varicella-zoster virus replication in culture, ex vivo, and in SCID-Hu mice.Antiviral research · 2010Article
- JNK and p38 mitogen-activated protein kinase pathways contribute to porcine circovirus type 2 infection.Journal of virology · 2009Article
- Alphaherpesvirus US3-mediated reorganization of the actin cytoskeleton is mediated by group A p21-activated kinases.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The transcription factors ATF-2 and c-Jun are important for transactivation of varicella-zoster virus (VZV) genes. c-Jun is activated by the c-Jun N-terminal kinase (JNK), a member of the mitogen-activated protein kinase pathway that responds to stress and cytokines. To study the effects of VZV on this pathway, confluent human foreskin fibroblasts were infected with cell-associated VZV for 1 to 4 days. Immunoblots showed that phosphorylated JNK and c-Jun levels increased in VZV-infected cells, and kinase assays determined that phospho-JNK was active. Phospho-JNK was detected after 24 h, and levels rose steadily over 4 days in parallel with accumulation of VZV antigen. The two main activators of JNK are MKK4 and MKK7, and levels of their active, phosphorylated forms also increased. The competitive inhibitor of JNK, SP600125, caused a dose-dependent reduction in VZV yield (50% effective concentration, congruent with 8 microM). Specificity was verified by immunoblotting; phospho-c-Jun was eliminated by 18 microM SP600125 in VZV-infected cells. Immunofluorescent confocal microscopy showed that phospho-c-Jun and most of phospho-JNK were in the nuclei of VZV-infected cells; some phospho-JNK was in the cytoplasm. MKK4, MKK7, JNK, and phospho-JNK were detected by immunoblotting in purified preparations of VZV virions, but c-Jun was absent. JNK was located in the virion tegument, as determined by biochemical fractionation and immunogold transmission electron microscopy. Overall, these results demonstrate the importance of the JNK pathway for VZV replication and advance the idea that JNK is a useful drug target against VZV.
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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.