ArticleJournal of virology2001
Interaction of the influenza virus nucleoprotein with the cellular CRM1-mediated nuclear export pathway.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers.
What it found
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Who cites it
156 citing papers in PubMed, 274 citations in OpenAlex.
- Small molecule inhibition of the mitochondrial lipid transfer protein STARD7 attenuates influenza viral replication.PLoS pathogens · 2026Article
- Host-Directed Antiviral Strategies Against Influenza Viruses: Host Targets, Multi-Omics Approaches and AI-Assisted Discovery.Veterinary sciences · 2026Review
- RANBP3 and RAN orchestrate CRM1-mediated nuclear export of hepatitis B virus RNAs.Journal of virology · 2026Article
- The genetic driver of Acute Necrotizing Encephalopathy, RANBP2, regulates the inflammatory response to Influenza A virus infection.Nature communications · 2026Article
- Broad-spectrum inhibition of influenza A virus replication by blocking the nuclear export of viral ribonucleoprotein complexes.Journal of virology · 2025Article
- Host Protein Kinase C⍺: The novel Mitogen Activated Protein Kinase (MAPK) specific scaffold regulating nuclear export of influenza virus ribonucleoprotein complexes.PLoS pathogens · 2025Article
- Concentration-dependent formation of intersegment interactions in the viral inclusions of influenza A virus infected cells.iScience · 2025Article
- Human MX1 orchestrates the cytoplasmic sequestration of neosynthesized influenza A virus vRNPs.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- PB2 and NP of North American H5N1 virus drive immune cell replication and systemic infections.Science advances · 2025Article
- Influenza A virus RNA localisation and the interceding trafficking pathways of the host cell.PLoS pathogens · 2025Review
- LDC000067, a CDK9 inhibitor, unveils promising results in suppressing influenza virus infectionsAntimicrobial agents and chemotherapy · 2025Article
- Unravelling the interaction between Influenza virus and the nuclear pore complex: insights into viral replication and host immune response.Virusdisease · 2024Review
- OTUB1 contributes to the stability and function of Influenza A virus NS2.PLoS pathogens · 2024Article
- Unveiling the role of host kinases at different steps of influenza A virus life cycle.Journal of virology · 2024Review
- Negative and ambisense RNA virus ribonucleocapsids: more than protective armor.Microbiology and molecular biology reviews : MMBR · 2023Review
- Viral Subversion of the Chromosome Region Maintenance 1 Export Pathway and Its Consequences for the Cell Host.Viruses · 2023Review
- Virus Infection and mRNA Nuclear Export.International journal of molecular sciences · 2023Review
- Article
- The Hierarchical Sequence Requirements of the H1 Subtype-Specific Noncoding Regions of Influenza A Virus.Microbiology spectrum · 2022Article
- An overview of influenza A virus genes, protein functions, and replication cycle highlighting important updates.Virus genes · 2022Review
96 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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza virus transcription occurs in the nuclei of infected cells, where the viral genomic RNAs are complexed with a nucleoprotein (NP) to form ribonucleoprotein (RNP) structures. Prior to assembly into progeny virions, these RNPs exit the nucleus and accumulate in the cytoplasm. The mechanisms responsible for RNP export are only partially understood but have been proposed to involve the viral M1 and NS2 polypeptides. We found that the drug leptomycin B (LMB), which specifically inactivates the cellular CRM1 polypeptide, caused nuclear retention of NP in virus-infected cells, indicating a role for the CRM1 nuclear export pathway in RNP egress. However, no alteration was seen in the cellular distribution of M1 or NS2, even in the case of a mutant virus which synthesizes greatly reduced amounts of NS2. Furthermore, NP was distributed throughout the nuclei of infected cells at early times postinfection but, when retained in the nucleus at late times by LMB treatment, was redistributed to the periphery of the nucleoplasm. No such change was seen in the nuclear distribution of M1 or NS2 after drug treatment. Similar to the behavior of NP, M1 and NS2 in infected cells, LMB treatment of cells expressing each polypeptide in isolation caused nuclear retention of NP but not M1 or NS2. Conversely, overexpression of CRM1 caused increased cytoplasmic accumulation of NP but had little effect on M1 or NS2 distribution. Consistent with this, NP bound CRM1 in vitro. Overall, these data raise the possibility that RNP export is mediated by a direct interaction between NP and the cellular CRM1 export pathway.
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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.