ArticleNature communications2023
mRNA 3'UTR lengthening by alternative polyadenylation attenuates inflammatory responses and correlates with virulence of Influenza A virus.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed, 16 citations in OpenAlex.
- The factory enters the fray: how mitochondrial protein trafficking shapes the host response to infection.Journal of virology · 2026Review
- Systematic dysregulation of immune-related alternative polyadenylation in systemic lupus erythematosus contributes to patient stratification.Journal of translational autoimmunity · 2026Article
- Multivariate GWAS reveals shared genetic basis of common oral diseases.Frontiers in genetics · 2026Article
- Alternative polyadenylation upon CPSF6 knock-out enhances HIV-1 infection in primary T cells.PLoS pathogens · 2025Article
- Article
- Knockdown of STK39 inhibits lung cancer brain metastasis by suppressing the CPSF4/NFκB/COX2 pathway.Journal of neuro-oncology · 2025Article
- Identification of RC3H1 as antiviral host factor binding to the non-structural protein 1 of Influenza A virus via a 3-stage computational pipeline and cell-based analysis.Virology journal · 2025Article
- Gene expression regulation and polyadenylation in ulcerative colitis via long-chain RNA sequencing.BMC genomics · 2025Article
- Fateful Decisions of Where to Cut the Line: Pathology Associated with Aberrant 3' End Processing and Transcription Termination.Journal of molecular biology · 2025Review
- Cellular RNA interacts with MAVS to promote antiviral signaling.Science (New York, N.Y.) · 2024Article
- Disruption of CPSF6 enhances cellular permissivity to HIV-1 infection through alternative polyadenylation.Research square · 2024Article
- Alternative mRNA polyadenylation regulates macrophage hyperactivation via the autophagy pathway.Cellular & molecular immunology · 2024Article
- Longitudinal Assessment of Nasopharyngeal Biomarkers Post-COVID-19: Unveiling Persistent Markers and Severity Correlations.Journal of proteome research · 2024Article
- Modulation of diverse biological processes by CPSF, the master regulator of mRNA 3' ends.RNA (New York, N.Y.) · 2024Review
- Antiviral responses versus virus-induced cellular shutoff: a game of thrones between influenza A virus NS1 and SARS-CoV-2 Nsp1.Frontiers in cellular and infection microbiology · 2024Review
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Changes of mRNA 3'UTRs by alternative polyadenylation (APA) have been associated to numerous pathologies, but the mechanisms and consequences often remain enigmatic. By combining transcriptomics, proteomics and recombinant viruses we show that all tested strains of IAV, including A/PR/8/34(H1N1) (PR8) and A/Cal/07/2009 (H1N1) (Cal09), cause APA. We mapped the effect to the highly conserved glycine residue at position 184 (G184) of the viral non-structural protein 1 (NS1). Unbiased mass spectrometry-based analyses indicate that NS1 causes APA by perturbing the function of CPSF4 and that this function is unrelated to virus-induced transcriptional shutoff. Accordingly, IAV strain PR8, expressing an NS1 variant with weak CPSF binding, does not induce host shutoff but only APA. However, recombinant IAV (PR8) expressing NS1(G184R) lacks binding to CPSF4 and thereby also the ability to cause APA. Functionally, the impaired ability to induce APA leads to an increased inflammatory cytokine production and an attenuated phenotype in a mouse infection model. Investigating diverse viral infection models showed that APA induction is a frequent ability of many pathogens. Collectively, we propose that targeting of the CPSF complex, leading to widespread alternative polyadenylation of host transcripts, constitutes a general immunevasion mechanism employed by a variety of pathogenic viruses.
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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.