ArticleScientific reports2018
SMARCA2-regulated host cell factors are required for MxA restriction of influenza A viruses.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Secondary analysis of influenza a virus-infected cells at single-cell resolution reveals host BANF1 response to individual and combinations of detected segments.Virology journal · 2026Article
- Integrative multi-omics analysisiScience · 2025Article
- Creation of a Novel Coding Program to Identify Genes Controlled by miRNAs During Human Rhinovirus Infection.Methods and protocols · 2025Article
- Heterozygous and generalist MxA super-restrictors overcome breadth-specificity trade-offs in antiviral restriction.Science advances · 2025Article
- Differential lung gene expression changes in C57BL/6 and DBA/2 mice carrying an identical functional Mx1 gene reveals crucial differences in the host response.BMC genomic data · 2024Article
- Identification of genetic biomarkers, drug targets and agents for respiratory diseases utilising integrated bioinformatics approaches.Scientific reports · 2023Article
- Proteomic and genetic analyses of influenza A viruses identify pan-viral host targets.Nature communications · 2023Article
- Cross-species analysis of viral nucleic acid interacting proteins identifies TAOKs as innate immune regulators.Nature communications · 2021Article
- BRD9 is a druggable component of interferon-stimulated gene expression and antiviral activity.EMBO reports · 2021Article
- Subcellular Localization of MxB Determines Its Antiviral Potential against Influenza A Virus.Journal of virology · 2020Article
- Mx genes: host determinants controlling influenza virus infection and trans-species transmission.Human genetics · 2020Review
- From APOBEC to ZAP: Diverse mechanisms used by cellular restriction factors to inhibit virus infections.Biochimica et biophysica acta. Molecular cell research · 2019Review
- Host and viral determinants of influenza A virus species specificity.Nature reviews. Microbiology · 2019Review
- Partial Inactivation of the Chromatin Remodelers SMARCA2 and SMARCA4 in Virus-Infected Cells by Caspase-Mediated Cleavage.Journal of virology · 2018Article
- Influenza A virus nucleoprotein is acetylated by histone acetyltransferases PCAF and GCN5.The Journal of biological chemistry · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
The human interferon (IFN)-induced MxA protein is a key antiviral host restriction factor exhibiting broad antiviral activity against many RNA viruses, including highly pathogenic avian influenza A viruses (IAV) of the H5N1 and H7N7 subtype. To date the mechanism for how MxA exerts its antiviral activity is unclear, however, additional cellular factors are believed to be essential for this activity. To identify MxA cofactors we performed a genome-wide siRNA-based screen in human airway epithelial cells (A549) constitutively expressing MxA using an H5N1 reporter virus. These data were complemented with a proteomic screen to identify MxA-interacting proteins. The combined data identified SMARCA2, the ATPase subunit of the BAF chromatin remodeling complex, as a crucial factor required for the antiviral activity of MxA against IAV. Intriguingly, our data demonstrate that although SMARCA2 is essential for expression of some IFN-stimulated genes (ISGs), and the establishment of an antiviral state, it is not required for expression of MxA, suggesting an indirect effect on MxA activity. Transcriptome analysis of SMARCA2-depleted A549-MxA cells identified a small set of SMARCA2-regulated factors required for activity of MxA, in particular IFITM2 and IGFBP3. These findings reveal that several virus-inducible factors work in concert to enable MxA restriction of IAV.
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Registered trials
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.