ArticleProceedings of the National Academy of Sciences of the United States of America2021
Cellular nucleic acid-binding protein is essential for type I interferon-mediated immunity to RNA virus infection.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- A highly prevalent lupus risk haplotype increases IRF7-dependent induction of IFN-α, enhancing antiviral defense and exacerbating autoimmunity.American journal of human genetics · 2026Article
- Cellular nucleic acid-binding protein (CNBP) dependent cytokine programming shapes host defense againstbioRxiv : the preprint server for biology · 2026Article
- RNA-binding proteins: a comprehensive review of multifaceted regulatory mechanisms in neuroinflammation and implications in the pathogenesis of neurological disorders.Journal of neuroinflammation · 2026Review
- A new candidate tumor suppressor tRF-Ser inhibits gastric cancer progression by regulating the CNBP/HSPA8 axis.Cell death & disease · 2026Article
- Article
- Dietary targeting of CNBP to rein in the EREG-EGFR cascade and restore homeostasis in colitis-associated colorectal cancer.International journal of biological sciences · 2026Article
- Viral polymerase-host interaction analysis reveals that the association between avian NUP93 and PB1 promotes H5N6 avian influenza virus replication.Microbiology spectrum · 2025Article
- CRISPR editing of candidate host factors that impact influenza A virus infection.Microbiology spectrum · 2025Article
- For Better or Worse: Type I Interferon Responses in Bacterial Infection.Pathogens (Basel, Switzerland) · 2025Review
- Proteomic Analysis of Differentially Expressed Proteins in A549 Cells Infected with H9N2 Avian Influenza Virus.International journal of molecular sciences · 2025Article
- Host Innate Antiviral Response to Influenza A Virus Infection: From Viral Sensing to Antagonism and Escape.Pathogens (Basel, Switzerland) · 2024Review
- The IRAK1/IRF5 axis initiates IL-12 response by dendritic cells and control of Toxoplasma gondii infection.Cell reports · 2024Article
- Virus versus host: influenza A virus circumvents the immune responses.Frontiers in microbiology · 2024Review
- Cellular nucleic acid-binding protein restricts SARS-CoV-2 by regulating interferon and disrupting RNA-protein condensates.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Sensing nucleotide composition in virus RNA.Bioscience reports · 2023Review
- Roles and functions of IAV proteins in host immune evasion.Frontiers in immunology · 2023Review
- Molecular mechanisms and cellular functions of liquid-liquid phase separation during antiviral immune responses.Frontiers in immunology · 2023Review
- Article
- Old and New Biomarkers for Infection, Inflammation, and Autoimmunity in Treatment-Resistant Affective and Schizophrenic Spectrum Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Type I interferons (IFNs) are innate immune cytokines required to establish cellular host defense. Precise control of IFN gene expression is crucial to maintaining immune homeostasis. Here, we demonstrated that cellular nucleic acid-binding protein (CNBP) was required for the production of type I IFNs in response to RNA virus infection. CNBP deficiency markedly impaired IFN production in macrophages and dendritic cells that were infected with a panel of RNA viruses or stimulated with synthetic double-stranded RNA. Furthermore, CNBP-deficient mice were more susceptible to influenza virus infection than were wild-type mice. Mechanistically, CNBP was phosphorylated and translocated to the nucleus, where it directly binds to the promoter of IFNb in response to RNA virus infection. Furthermore, CNBP controlled the recruitment of IFN regulatory factor (IRF) 3 and IRF7 to IFN promoters for the maximal induction of IFNb gene expression. These studies reveal a previously unrecognized role for CNBP as a transcriptional regulator of type I IFN genes engaged downstream of RNA virus-mediated innate immune signaling, which provides an additional layer of control for IRF3- and IRF7-dependent type I IFN gene expression and the antiviral innate immune response.
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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.