ArticleScience translational medicine2012
Productive replication of Ebola virus is regulated by the c-Abl1 tyrosine kinase.
Article in Science translational medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 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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Who cites it
80 citing papers in PubMed, 126 citations in OpenAlex.
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- Role of c-ABL in DENV-2 Infection and Actin Remodeling in Vero Cells.International journal of molecular sciences · 2025Article
- ZIKV prM hijacks PIM1 kinase for phosphorylation to prevent ubiquitin-mediated degradation and facilitate viral replication.Frontiers in cellular and infection microbiology · 2024Article
- Repurposing clinically available drugs and therapies for pathogenic targets to combat SARS-CoV-2.MedComm · 2023Review
- Cheminformatics-Based Study Identifies Potential Ebola VP40 Inhibitors.International journal of molecular sciences · 2023Article
- Review
- Identification of oral therapeutics using an AI platform against the virus responsible for COVID-19, SARS-CoV-2.Frontiers in pharmacology · 2023Article
- Imatinib inhibits SARS-CoV-2 infection by an off-target-mechanism.Scientific reports · 2022Article
- Kinase Inhibitors as Potential Therapeutic Agents in the Treatment of COVID-19.Frontiers in pharmacology · 2022Review
- Effective Antiviral Activity of the Tyrosine Kinase Inhibitor Sunitinib Malate against Zika Virus.Infection & chemotherapy · 2021Article
- Lipid-protein interactions in virus assembly and budding from the host cell plasma membrane.Biochemical Society transactions · 2021Review
- P300-mediated NEDD4 acetylation drives ebolavirus VP40 egress by enhancing NEDD4 ligase activity.PLoS pathogens · 2021Article
- Pharmacological Modulators of Autophagy as a Potential Strategy for the Treatment of COVID-19.International journal of molecular sciences · 2021Review
- Antiviral drug screen identifies DNA-damage response inhibitor as potent blocker of SARS-CoV-2 replication.Cell reports · 2021Article
- Identification of Unique Peptides for SARS-CoV-2 Diagnostics and Vaccine Development by anFrontiers in immunology · 2021Article
- Strategy, Progress, and Challenges of Drug Repurposing for Efficient Antiviral Discovery.Frontiers in pharmacology · 2021Review
- A Novel Ebola Virus VP40 Matrix Protein-Based Screening for Identification of Novel Candidate Medical Countermeasures.Viruses · 2020Article
- Repurposing anticancer drugs for the management of COVID-19.European journal of cancer (Oxford, England : 1990) · 2020Review
- COVID-19 therapy: What weapons do we bring into battle?Bioorganic & medicinal chemistry · 2020Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Ebola virus causes a fulminant infection in humans resulting in diffuse bleeding, vascular instability, hypotensive shock, and often death. Because of its high mortality and ease of transmission from human to human, Ebola virus remains a biological threat for which effective preventive and therapeutic interventions are needed. An understanding of the mechanisms of Ebola virus pathogenesis is critical for developing antiviral therapeutics. Here, we report that productive replication of Ebola virus is modulated by the c-Abl1 tyrosine kinase. Release of Ebola virus-like particles (VLPs) in a cell culture cotransfection system was inhibited by c-Abl1-specific small interfering RNA (siRNA) or by Abl-specific kinase inhibitors and required tyrosine phosphorylation of the Ebola matrix protein VP40. Expression of c-Abl1 stimulated an increase in phosphorylation of tyrosine 13 (Y(13)) of VP40, and mutation of Y(13) to alanine decreased the release of Ebola VLPs. Productive replication of the highly pathogenic Ebola virus Zaire strain was inhibited by c-Abl1-specific siRNAs or by the Abl-family inhibitor nilotinib by up to four orders of magnitude. These data indicate that c-Abl1 regulates budding or release of filoviruses through a mechanism involving phosphorylation of VP40. This step of the virus life cycle therefore may represent a target for antiviral therapy.
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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.