ArticleThe FEBS journal2014
Influenza A viral nucleoprotein interacts with cytoskeleton scaffolding protein α-actinin-4 for viral replication.
Article in The FEBS journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 48 citations in OpenAlex.
- Article
- SOCS1 depletion drives osteosarcoma stemness and chemoresistance by suppressing ACTN4 degradation.Acta pharmacologica Sinica · 2026Article
- Characterization of ACTN4 as a novel antiviral target against SARS-CoV-2.Signal transduction and targeted therapy · 2024Article
- LINC01002 functions as a ceRNA to regulate FRMD8 by sponging miR-4324 for the development of COVID-19.Virology journal · 2024Article
- Avian Influenza A Viruses Modulate the Cellular Cytoskeleton during Infection of Mammalian Hosts.Pathogens (Basel, Switzerland) · 2024Review
- Multi-omics analysis reveals the impact of influenza a virus host adaptation on immune signatures in pig tracheal tissue.Frontiers in immunology · 2024Article
- Alpha-actnin-4 (ACTN4) selectively affects the DNA double-strand breaks repair in non-small lung carcinoma cells.Biology direct · 2022Article
- Interaction of Influenza A Nucleoprotein with Host hnRNP-C Is Implicated in Viral Replication.International journal of molecular sciences · 2022Article
- ILDR1 promotes influenza A virus replication through binding to PLSCR1.Scientific reports · 2022Article
- Interaction of influenza A virus NS1 and cytoskeleton scaffolding protein α-actinin 4.Virus genes · 2022Article
- Article
- Role of ARP2/3 Complex-Driven Actin Polymerization in RSV Infection.Pathogens (Basel, Switzerland) · 2021Review
- Acetylation, Methylation and Allysine Modification Profile of Viral and Host Proteins during Influenza A Virus Infection.Viruses · 2021Article
- Influenza A Virus: Host-Virus Relationships.Viruses · 2020Article
- Upregulation of miR-101 during Influenza A Virus Infection Abrogates Viral Life Cycle by Targeting mTOR Pathway.Viruses · 2020Article
- Influenza A Virus Nucleoprotein Activates the JNK Stress-Signaling Pathway for Viral Replication by Sequestering Host Filamin A Protein.Frontiers in microbiology · 2020Article
- Prediction of repurposed drugs for treating lung injury in COVID-19.F1000Research · 2020Article
- Review
- The actin cytoskeleton is important for rotavirus internalization and RNA genome replication.Virus research · 2019Article
- Histone acetyl transferase TIP60 inhibits the replication of influenza a virus by activation the TBK1-IRF3 pathway.Virology journal · 2018Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A virus (IAV), similar to other viruses, exploits the machinery of human host cells for its survival and replication. We identified α-actinin-4, a host cytoskeletal protein, as an interacting partner of IAV nucleoprotein (NP). We confirmed this interaction using co-immunoprecipitation studies, first in a coupled in vitro transcription-translation assay and then in cells either transiently co-expressing the two proteins or infected with whole IAV. Importantly, the NP-actinin-4 interaction was observed in several IAV subtypes, including the 2009 H1N1 pandemic virus. Moreover, immunofluorescence studies revealed that both NP and actinin-4 co-localized largely around the nucleus and also in the cytoplasmic region of virus-infected A549 cells. Silencing of actinin-4 expression resulted in not only a significant decrease in NP, M2 and NS1 viral protein expression, but also a reduction of both NP mRNA and viral RNA levels, as well as viral titers, 24 h post-infection with IAV, suggesting that actinin-4 was critical for viral replication. Furthermore, actinin-4 depletion reduced the amount of NP localized in the nucleus. Treatment of infected cells with wortmannin, a known inhibitor of actinin-4, led to a decrease in NP mRNA levels and also caused the nuclear retention of NP, further strengthening our previous observations. Taken together, the results of the present study indicate that actinin-4, a novel interacting partner of IAV NP, plays a crucial role in viral replication and this interaction may participate in nuclear localization of NP and/or viral ribonucleoproteins.
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