ArticleOncotarget2016
The epidermal growth factor receptor regulates cofilin activity and promotes transmissible gastroenteritis virus entry into intestinal epithelial cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
39 citing papers in PubMed, 55 citations in OpenAlex.
- Activities of fungal metabolites sphaeropsidin A and B to fight against canine coronavirus.Veterinary research communications · 2026Article
- Cell entry mechanisms of porcine enteric coronaviruses.The Journal of biological chemistry · 2026Review
- Alpha-dystroglycan receptor signaling likely influences basement membrane laminin α2 mediated pathology in the stria vascularis of Alport mice.Hearing research · 2025Article
- Molecular docking as a tool for the discovery of novel insight about the role of acid sphingomyelinase inhibitors in SARS- CoV-2 infectivity.BMC public health · 2024Review
- A role for tunneling nanotubes in virus spread.Frontiers in microbiology · 2024Review
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- Coronavirus and the Cytoskeleton of Virus-Infected Cells.Sub-cellular biochemistry · 2023Article
- Review
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- Screening Host Antiviral Proteins under the Enhanced Immune Responses Induced by a Variant Strain of Porcine Epidemic Diarrhea Virus.Microbiology spectrum · 2022Article
- The Effects of Swine Coronaviruses on ER Stress, Autophagy, Apoptosis, and Alterations in Cell Morphology.Pathogens (Basel, Switzerland) · 2022Review
- Article
- Cortactin in Lung Cell Function and Disease.International journal of molecular sciences · 2022Review
- Virus interactions with the actin cytoskeleton-what we know and do not know about SARS-CoV-2.Archives of virology · 2022Review
- The Epidermal Growth Factor Receptor Is a Relevant Host Factor in the Early Stages of The Zika Virus Life CycleJournal of virology · 2021Article
- The Interference between SARS-CoV-2 and Tyrosine Kinase Receptor Signaling in Cancer.International journal of molecular sciences · 2021Review
- Microfilaments and microtubules alternately coordinate the multi-step endosomal trafficking of Classical Swine Fever Virus.Journal of virology · 2021Article
- Rapid and Efficient Cell-to-Cell Transmission of Avian Influenza H5N1 Virus in MDCK Cells Is Achieved by Trogocytosis.Pathogens (Basel, Switzerland) · 2021Article
- Cell Division Control Protein 42 Interacts With Hepatitis E Virus Capsid Protein and Participates in Hepatitis E Virus Infection.Frontiers in microbiology · 2021Article
- Hsp90 Inhibitors Inhibit the Entry of Herpes Simplex Virus 1 Into Neuron Cells by Regulating Cofilin-Mediated F-Actin Reorganization.Frontiers in microbiology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transmissible gastroenteritis virus (TGEV), a coronavirus, causes severe diarrhea and high mortality in newborn piglets. The porcine intestinal epithelium is the target of TGEV infection, but the mechanisms that TGEV disrupts the actin cytoskeleton and invades the host epithelium remain largely unknown. We not only found that TGEV infection stimulates F-actin to gather at the cell membrane but the disruption of F-actin inhibits TGEV entry as well. Cofilin is involved in F-actin reorganization and TGEV entry. The TGEV spike protein is capable of binding with EGFR, activating the downstream phosphoinositide-3 kinase (PI3K), then causing the phosphorylation of cofilin and F-actin polymerization via Rac1/Cdc42 GTPases. Inhibition of EGFR and PI3K decreases the entry of TGEV. EGFR is also the upstream activator of mitogen-activated protein kinase (MAPK) signaling pathways that is involved in F-actin reorganization. Additionally, lipid rafts act as signal platforms for the EGFR-associated signaling cascade and correlate with the adhesion of TGEV. In conlusion, these results provide valuable data of the mechanisms which are responsible for the TGEV pathogenesis and may lead to the development of new methods about controlling TGEV.
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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.