ArticleNature communications2022
Ebola virus VP35 hijacks the PKA-CREB1 pathway for replication and pathogenesis by AKIP1 association.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Molecular Insights into High-Pathogenicity RNA Viruses.Viruses · 2026Review
- Integration of ATAC-seq and RNA-seq analysis identifies host genes related with PRRSV infection.Veterinary research · 2026Article
- Poxvirus infection triggers remodeling of host m⁶A epitranscriptome and benefits from the m⁶A regulatory responses.Virology journal · 2026Article
- 25 Years of Ebola Virus VP35 Research.Journal of molecular biology · 2025Review
- CRTC3 restricts SARS-CoV-2 replication and is antagonized by CREB.Virologica Sinica · 2025Article
- The PKA-CREB1 axis regulates coronavirus proliferation by viral helicase nsp13 association.Journal of virology · 2024Article
- Ebola virus VP35 interacts non-covalently with ubiquitin chains to promote viral replication.PLoS biology · 2024Article
- Article
- Navigating the Complex Landscape of Ebola Infection Treatment: A Review of Emerging Pharmacological Approaches.Infectious diseases and therapy · 2024Review
- ZIKV prM hijacks PIM1 kinase for phosphorylation to prevent ubiquitin-mediated degradation and facilitate viral replication.Frontiers in cellular and infection microbiology · 2024Article
- Aptamers: precision tools for diagnosing and treating infectious diseases.Frontiers in cellular and infection microbiology · 2024Review
- Sustained CREB phosphorylation by lipid-peptide liquid crystalline nanoassemblies.Communications chemistry · 2023Article
- High-efficiency genetic engineering toolkit for virus based on lambda red-mediated recombination.Biotechnology letters · 2023Article
- Ebola Virus VP35 Interacts Non-Covalently with Ubiquitin Chains to Promote Viral Replication Creating New Therapeutic Opportunities.bioRxiv : the preprint server for biology · 2023Article
- Spatial and functional arrangement of Ebola virus polymerase inside phase-separated viral factories.Nature communications · 2023Article
- Highly pathogenic coronavirus N protein aggravates inflammation by MASP-2-mediated lectin complement pathway overactivation.Signal transduction and targeted therapy · 2022Article
Corrections and comments
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Authors and funding
28 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ebola virus (EBOV), one of the deadliest viruses, is the cause of fatal Ebola virus disease (EVD). The underlying mechanism of viral replication and EBOV-related hemorrhage is not fully understood. Here, we show that EBOV VP35, a cofactor of viral RNA-dependent RNA polymerase, binds human A kinase interacting protein (AKIP1), which consequently activates protein kinase A (PKA) and the PKA-downstream transcription factor CREB1. During EBOV infection, CREB1 is recruited into EBOV ribonucleoprotein complexes in viral inclusion bodies (VIBs) and employed for viral replication. AKIP1 depletion or PKA-CREB1 inhibition dramatically impairs EBOV replication. Meanwhile, the transcription of several coagulation-related genes, including THBD and SERPINB2, is substantially upregulated by VP35-dependent CREB1 activation, which may contribute to EBOV-related hemorrhage. The finding that EBOV VP35 hijacks the host PKA-CREB1 signal axis for viral replication and pathogenesis provides novel potential therapeutic approaches against EVD.
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