ArticleCell host & microbe2013
An ERK-p38 subnetwork coordinates host cell apoptosis and necrosis during coxsackievirus B3 infection.
Article in Cell host & microbe, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 45 citations in OpenAlex.
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- Therapeutic Targeting of Viral Myocarditis with Natural Products and Herbal Medicines: From Immune-Inflammatory Mechanisms to Clinical Translation.Journal of inflammation research · 2026Review
- Study on the inhibitory effect of geniposide on coxsackievirus and its mechanism.Frontiers in pharmacology · 2026Article
- Protein deglycase DJ-1 deficiency aggravates acute viral myocarditis by promoting apoptosis via reducing Dusp1 expression.Cell death & disease · 2025Article
- Transcriptomic analysis of coxsackievirus B3 infection in induced pluripotent stem cell-derived brain-like endothelial cells.Journal of virology · 2025Article
- Polycomb Repressive Complex 2 promotes atherosclerotic plaque vulnerability.bioRxiv : the preprint server for biology · 2024Article
- Picornavirus security proteins promote the release of extracellular vesicle enclosed viruses via the modulation of host kinases.PLoS pathogens · 2024Article
- Phosphorylation of enteroviral 2AJournal of medical virology · 2023Article
- Advances in cell death mechanisms involved in viral myocarditis.Frontiers in cardiovascular medicine · 2022Review
- Transcriptomic analysis reveals that coxsackievirus B3 Woodruff and GD strains use similar key genes to induce FoxO signaling pathway activation in HeLa cells.Archives of virology · 2022Article
- ERK5 signalling pathway is a novel target of sorafenib: Implication in EGF biology.Journal of cellular and molecular medicine · 2021Article
- Modeling the complete kinetics of coxsackievirus B3 reveals human determinants of host-cell feedback.Cell systems · 2021Article
- Conditional ablation of MAPK7 expression in chondrocytes impairs endochondral bone formation in limbs and adaptation of chondrocytes to hypoxia.Cell & bioscience · 2020Article
- Cleavage of Desmosomal Cadherins Promotes γ-Catenin Degradation and Benefits Wnt Signaling in Coxsackievirus B3-Induced Destruction of Cardiomyocytes.Frontiers in microbiology · 2020Article
- Robust latent-variable interpretation of in vivo regression models by nested resampling.Scientific reports · 2019Article
- An ultrasensitive fiveplex activity assay for cellular kinases.Scientific reports · 2019Article
- Association of Intestinal Alkaline Phosphatase With Necrotizing Enterocolitis Among Premature Infants.JAMA network open · 2019Article
- p38-mediated phosphorylation at T367 induces EZH2 cytoplasmic localization to promote breast cancer metastasis.Nature communications · 2018Article
- Systems analysis of latent HIV reversal reveals altered stress kinase signaling and increased cell death in infected T cells.Scientific reports · 2017Article
- Profiling Subcellular Protein Phosphatase Responses to Coxsackievirus B3 Infection of Cardiomyocytes.Molecular & cellular proteomics : MCP · 2017Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
The host response to a virus is determined by intracellular signaling pathways that are modified during infection. These pathways converge as networks and produce interdependent phenotypes, making it difficult to link virus-induced signals and responses at a systems level. Coxsackievirus B3 (CVB3) infection induces death of cardiomyocytes, causing tissue damage and virus dissemination, through incompletely characterized host cell signaling networks. We built a statistical model that quantitatively predicts cardiomyocyte responses from time-dependent measurements of phosphorylation events modified by CVB3. Model analysis revealed that CVB3-stimulated cytotoxicity involves tight coupling between the host ERK and p38 MAPK pathways, which are generally thought to control distinct cellular responses. The kinase ERK5 requires p38 kinase activity and inhibits apoptosis caused by CVB3 infection. By contrast, p38 indirectly promotes apoptosis via ERK1/2 inhibition but directly causes CVB3-induced necrosis. Thus, the cellular events governing pathogenesis are revealed when virus-host programs are monitored systematically and deconvolved mathematically.
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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.