ArticleFrontiers in microbiology2020
Influenza A Virus Nucleoprotein Activates the JNK Stress-Signaling Pathway for Viral Replication by Sequestering Host Filamin A Protein.
Article in Frontiers in microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- HEV replication is promoted by blocking the NF-κB signaling pathway through inhibiting FLNa expression.Journal of virology · 2026Article
- Lung-specific CRBN knockout attenuates influenza a virus-induced acute lung injury in mice: a potential therapeutic approach.BMC infectious diseases · 2025Article
- Influenza-induced microRNA-155 expression is altered in extracellular vesicles derived from the COPD epithelium.Frontiers in cellular and infection microbiology · 2025Article
- The potential of ARL4C and its-mediated genes in atherosclerosis and agent development.Frontiers in pharmacology · 2025Review
- Filamin B restricts vaccinia virus spread and is targeted by vaccinia virus protein C4.Journal of virology · 2024Article
- The nucleoprotein of influenza A virus inhibits the innate immune response by inducing mitophagy.Autophagy · 2023Article
- Protein-Coding Region Derived Small RNA in Exosomes from Influenza A Virus-Infected Cells.International journal of molecular sciences · 2023Article
- Arctiin suppresses H9N2 avian influenza virus-mediated inflammation via activation of Nrf2/HO-1 signaling.BMC complementary medicine and therapies · 2021Article
- Cytoskeleton and Associated Proteins: Pleiotropic JNK Substrates and Regulators.International journal of molecular sciences · 2021Review
- Acetylation, Methylation and Allysine Modification Profile of Viral and Host Proteins during Influenza A Virus Infection.Viruses · 2021Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A virus (IAV) poses a major threat to global public health and is known to employ various strategies to usurp the host machinery for survival. Due to its fast-evolving nature, IAVs tend to escape the effect of available drugs and vaccines thus, prompting the development of novel antiviral strategies. High-throughput mass spectrometric screen of host-IAV interacting partners revealed host Filamin A (FLNA), an actin-binding protein involved in regulating multiple signaling pathways, as an interaction partner of IAV nucleoprotein (NP). In this study, we found that the IAV NP interrupts host FLNA-TRAF2 interaction by interacting with FLNA thus, resulting in increased levels of free, displaced TRAF2 molecules available for TRAF2-ASK1 mediated JNK pathway activation, a pathway critical to maintaining efficient viral replication. In addition, siRNA-mediated FLNA silencing was found to promote IAV replication (87% increase) while FLNA-overexpression impaired IAV replication (65% decrease). IAV NP was observed to be a crucial viral factor required to attain FLNA mRNA and protein attenuation post-IAV infection for efficient viral replication. Our results reveal FLNA to be a host factor with antiviral potential hitherto unknown to be involved in the IAV replication cycle thus, opening new possibilities of FLNA-NP interaction as a candidate anti-influenza drug development target.
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