ArticleJournal of virology2007
The ERK mitogen-activated protein kinase pathway contributes to Ebola virus glycoprotein-induced cytotoxicity.
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 44 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 71 citations in OpenAlex.
- Early activation of p38 mitogen activated protein kinase is associated with interferon-alpha-induced depression and fatigue.Brain, behavior, and immunity · 2011Trial
- White Spot Syndrome Virus Envelope Protein VP53B Functions as a Trypsin Inhibitor and Interacts With Hemocyanin.Journal of fish diseases · 2026Article
- Ebola virus exploits host lncRNAbioRxiv : the preprint server for biology · 2026Article
- Host-virus miRNA crosstalk in ebola virus disease.Folia microbiologica · 2026Review
- Review
- Identification and Potential Roles of Human MicroRNAs in Ebola Virus Infection and Disease Pathogenesis.Genes · 2024Article
- The Modulation of Immune Responses inViruses · 2023Article
- Influenza A virus replication has a stronger dependency on Raf/MEK/ERK signaling pathway activity than SARS-CoV-2.Frontiers in cellular and infection microbiology · 2023Article
- The MEK1/2-inhibitor ATR-002 efficiently blocks SARS-CoV-2 propagation and alleviates pro-inflammatory cytokine/chemokine responses.Cellular and molecular life sciences : CMLS · 2022Article
- Article
- Activation of the extracellular signal-regulated kinase pathway is required for replication of Newcastle disease virus.Archives of virology · 2021Article
- Development of a Multivalent Kunjin Virus Reporter Virus-Like Particle System Inducing Seroconversion for Ebola and West Nile Virus Proteins in Mice.Microorganisms · 2020Article
- Repurposing of Kinase Inhibitors for Treatment of COVID-19.Pharmaceutical research · 2020Review
- Article
- Porcine deltacoronavirus activates the Raf/MEK/ERK pathway to promote its replication.Virus research · 2020Article
- Global phosphoproteomic analysis of Ebola virions reveals a novel role for VP35 phosphorylation-dependent regulation of genome transcription.Cellular and molecular life sciences : CMLS · 2020Article
- Article
- Kinetics of Soluble Mediators of the Host Response in Ebola Virus Disease.The Journal of infectious diseases · 2018Article
- Ebolaviruses: New roles for old proteins.PLoS neglected tropical diseases · 2018Review
- Repurposing of Kinase Inhibitors as Broad-Spectrum Antiviral Drugs.DNA and cell biology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
Ebola virus is a highly lethal pathogen that causes hemorrhagic fever in humans and nonhuman primates. Among the seven known viral gene products, the envelope glycoprotein (GP) alone induces cell rounding and detachment that ultimately leads to cell death. Cellular cytoxicity is not seen with comparable levels of expression of a mutant form of GP lacking a mucin-like domain (GPDeltamuc). GP-induced cell death is nonapoptotic and is preceded by downmodulation of cell surface molecules involved in signaling pathways, including certain integrins and epidermal growth factor receptor. To investigate the mechanism of GP-induced cellular toxicity, we analyzed the activation of several signal transduction pathways involved in cell growth and survival. The active form of extracellular signal-regulated kinases types 1 and 2 (ERK1/2), phospho-ERK1/2, was reduced in cells expressing GP compared to those expressing GPDeltamuc as determined by flow cytometry, in contrast to the case for several other signaling proteins. Subsequent analysis of the activation states and kinase activities of related kinases revealed a more pronounced effect on the ERK2 kinase isoform. Disruption of ERK2 activity by a dominant negative ERK or by small interfering RNA-mediated ERK2 knockdown potentiated the decrease in alphaV integrin expression associated with toxicity. Conversely, activation of the pathway through the expression of a constitutively active form of ERK2 significantly protected against this effect. These results indicate that the ERK signaling cascade mediates GP-mediated cytotoxicity and plays a role in pathogenicity induced by this gene product.
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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.