ArticleThe Journal of biological chemistry2012
Transport of influenza virus neuraminidase (NA) to host cell surface is regulated by ARHGAP21 and Cdc42 proteins.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 75 citations in OpenAlex.
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- A small protein encoded by PCBP1-AS1 is identified as a key regulator of influenza virus replication via enhancing autophagy.PLoS pathogens · 2024Article
- Phylogenetic identification of influenza virus candidates for seasonal vaccines.Science advances · 2023Article
- Impact of actin polymerization and filopodia formation on herpes simplex virus entry in epithelial, neuronal, and T lymphocyte cells.Frontiers in cellular and infection microbiology · 2023Review
- A Novel lncRNA SAAL Suppresses IAV Replication by Promoting Innate Responses.Microorganisms · 2022Article
- I226R Protein of African Swine Fever Virus Is a Suppressor of Innate Antiviral Responses.Viruses · 2022Article
- Long Noncoding RNA IFITM4P Regulates Host Antiviral Responses by Acting as a Competing Endogenous RNA.Journal of virology · 2021Article
- Role of PDZ-binding motif from West Nile virus NS5 protein on viral replication.Scientific reports · 2021Article
- Human Properdin Released By Infiltrating Neutrophils Can Modulate Influenza A Virus Infection.Frontiers in immunology · 2021Article
- Comprehensive Transcriptomic Analysis Identifies Novel Antiviral Factors Against Influenza A Virus Infection.Frontiers in immunology · 2021Article
- Screening for Anti-Inflammation Quality Markers of Lianhua Qingwen Capsule Based on Network Pharmacology, UPLC, and Biological Activity.Frontiers in pharmacology · 2021Article
- RDUR, a lncRNA, Promotes Innate Antiviral Responses and Provides Feedback Control of NF-κB Activation.Frontiers in immunology · 2021Article
- Article
- A Long Non-coding RNA IVRPIE Promotes Host Antiviral Immune Responses Through Regulating Interferon β1 and ISG Expression.Frontiers in microbiology · 2020Article
- Zinc Finger CCCH-Type Antiviral Protein 1 Restricts the Viral Replication by Positively Regulating Type I Interferon Response.Frontiers in microbiology · 2020Article
- Complement-Independent Modulation of Influenza A Virus Infection by Factor H.Frontiers in immunology · 2020Article
- Experimental validation and computational modeling of anti-influenza effects of quercetin-3-O-α-L-rhamnopyranoside from indigenous south African medicinal plant Rapanea melanophloeos.BMC complementary and alternative medicine · 2019Article
- Review
- Influenza Virus-Induced Robust Expression of SOCS3 Contributes to Excessive Production of IL-6.Frontiers in immunology · 2019Article
- Interaction of Abl Tyrosine Kinases with SOCS3 Impairs Its Suppressor Function in Tumorigenesis.Neoplasia (New York, N.Y.) · 2018Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza virus neuraminidase (NA) is transported to the virus assembly site at the plasma membrane and is a major viral envelope component that plays a critical role in the release of progeny virions and in determination of host range restriction. However, little is known about the host factors that are involved in regulating the intracellular and cell surface transport of NA. Here we identified the Cdc42-specific GAP, ARHGAP21 differentially expressed in host cells infected with influenza A virus using cDNA microarray analysis. Furthermore, we have investigated the involvement of Rho family GTPases in NA transport to the cell surface. We found that expression of constitutively active or inactive mutants of RhoA or Rac1 did not significantly affect the amount of NA that reached the cell surface. However, expression of constitutively active Cdc42 or depletion of ARHGAP21 promoted the transport of NA to the plasma membranes. By contrast, cells expressing shRNA targeting Cdc42 or overexpressing ARHGAP21 exhibited a significant decrease in the amount of cell surface-localized NA. Importantly, silencing Cdc42 reduced influenza A virus replication, whereas silencing ARHGAP21 increased the virus replication. Together, our results reveal that ARHGAP21- and Cdc42-based signaling regulates the NA transport and thereby impacts virus replication.
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