ArticleNature communications2019
A genome-wide CRISPR screen identifies N-acetylglucosamine-1-phosphate transferase as a potential antiviral target for Ebola virus.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 73 citations in OpenAlex.
- S100A11 regulates hepatic cholesterol metabolism and promotes steatohepatitis via noncanonical SREBP2 signaling.The Journal of clinical investigation · 2026Article
- Genome-wide CRISPR screen reveals PEX11B as a host restriction factor against ORFV through membrane fluidity regulation.PLoS pathogens · 2026Article
- From CRISPR functional genomics to synthetic interventions: engineering antiviral strategies.Journal of virology · 2026Review
- Meta-analysis of functional genomics studies reveals conserved cellular pathways required by viruses of pandemic concern.Access microbiology · 2026Article
- Knowledge graph and machine learning-guided virtual screening prioritizes putative blockers of the PSMD11/Rpn6-EBOV glycoprotein interface.Frontiers in pharmacology · 2026Article
- Targeting Host Dependency Factors: A Paradigm Shift in Antiviral Strategy Against RNA Viruses.International journal of molecular sciences · 2025Review
- Replicon-based genome-wide CRISPR knockout screening for the identification of host factors involved in viral replication.Nature communications · 2025Article
- A protein-proximity screen reveals Ebola virus co-opts the mRNA decapping complex through the scaffold protein EDC4.Nature communications · 2025Article
- Article
- Tau uptake by human neurons depends on receptor LRP1 and kinase LRRK2.The EMBO journal · 2025Article
- Defining the host dependencies and the transcriptional landscape of RSV infection and bystander activation.bioRxiv : the preprint server for biology · 2025Article
- Single-cell image-based screens identify host regulators of Ebola virus infection dynamics.Nature microbiology · 2025Article
- Cathepsins in cellular entry of human pathogenic viruses.Journal of virology · 2025Review
- Review
- Genome-wide CRISPR/Cas9 screen identifies SLC39A9 and PIK3C3 as crucial entry factors for Ebola virus infection.PLoS pathogens · 2024Article
- Hepatitis E Virus: What More Do We Need to Know?Medicina (Kaunas, Lithuania) · 2024Review
- Crimean-Congo haemorrhagic fever virus uses LDLR to bind and enter host cells.Nature microbiology · 2024Article
- Mapping of susceptibility loci for Ebola virus pathogenesis in mice.Cell reports · 2024Article
- Single-cell image-based genetic screens systematically identify regulators of Ebola virus subcellular infection dynamics.bioRxiv : the preprint server for biology · 2024Article
- Navigating the Complex Landscape of Ebola Infection Treatment: A Review of Emerging Pharmacological Approaches.Infectious diseases and therapy · 2024Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
There are no approved therapies for Ebola virus infection. Here, to find potential therapeutic targets, we perform a screen for genes essential for Ebola virus (EBOV) infection. We identify GNPTAB, which encodes the α and β subunits of N-acetylglucosamine-1-phosphate transferase. We show that EBOV infection of a GNPTAB knockout cell line is impaired, and that this is reversed by reconstituting GNPTAB expression. Fibroblasts from patients with mucolipidosis II, a disorder associated with mutations in GNPTAB, are refractory to EBOV, whereas cells from their healthy parents support infection. Impaired infection correlates with loss of the expression of cathepsin B, known to be essential for EBOV entry. GNPTAB activity is dependent upon proteolytic cleavage by the SKI-1/S1P protease. Inhibiting this protease with the small-molecule PF-429242 blocks EBOV entry and infection. Disruption of GNPTAB function may represent a strategy for a host-targeted therapy for EBOV.
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