ArticleImmunobiology2017
Schlafen 14 (SLFN14) is a novel antiviral factor involved in the control of viral replication.
Article in Immunobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
40 citing papers in PubMed, 47 citations in OpenAlex.
- Type II tRNA cleavage by SLFN14 endoribonuclease variants linked to inherited thrombocytopenia drives global translational repression.PLoS biology · 2026Article
- Rapid Production of Recombinant Human SLFN14 Ribonuclease and Stoichiometric Analysis by Mass Photometry.Journal of visualized experiments : JoVE · 2026Article
- SLFN14 functions as a P-TEFb inhibitor to modulate the transcription of HIV-1 and cellular genes.Science advances · 2025Article
- Epigenetic and Post-Translational Regulation of Schlafen Family Expression and Their Differential Methods of Regulating Proteins.International journal of molecular sciences · 2025Review
- Schlafen 12 Modulation and Targeting in Acute Myeloid Leukemia.Cancer research communications · 2025Article
- Human Schlafen 14 Cleavage of Short Double-Stranded RNAs Underpins its Antiviral Activity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Recurrent Evolutionary Innovations in Rodent and Primate Schlafen Genes.Genome biology and evolution · 2025Article
- Multi-proteomic profiling of the varicella-zoster virus-host interface reveals host susceptibilities to severe infection.Nature microbiology · 2025Article
- CryoEM structure of the SLFN14 endoribonuclease reveals insight into RNA binding and cleavage.Nature communications · 2025Article
- Structural and functional characterization of human SLFN14.Nucleic acids research · 2025Article
- Review
- Article
- Influenza Virus Host Restriction Factors: The ISGs and Non-ISGs.Pathogens (Basel, Switzerland) · 2024Review
- Comparative transcriptome analysis of T lymphocyte subpopulations and identification of critical regulators defining porcine thymocyte identity.Frontiers in immunology · 2024Article
- Article
- "Transfer" of power: The intersection of DNA virus infection and tRNA biology.Seminars in cell & developmental biology · 2023Review
- Human Schlafen 11 inhibits influenza A virus production.Virus research · 2023Article
- Structural and biochemical characterization of Schlafen11 N-terminal domain.Nucleic acids research · 2023Article
- Schlafen 12 restricts HIV-1 latency reversal by a codon-usage dependent post-transcriptional block in CD4+ T cells.Communications biology · 2023Article
- Velcrin-induced selective cleavage of tRNANature chemical biology · 2023Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Schlafen (SLFN) proteins have been suggested to play important functions in cell proliferation and immune cell development. In this study, we determined the antiviral activities of putative RNA-helicase domain-containing SLFN14. Murine SLFN14 expression was specifically induced by TLR3-mediated pathways and type I interferon (IFN) in RAW264.7 mouse macrophages. To examine the role of SLFN during viral infection, cells were infected with either wild-type PR8 or delNS1/PR8 virus. SLFN14 expression was specifically induced following influenza virus infection. Overexpression of SLFN14 in A549 cells reduced viral replication, whereas knockdown of SLFN14 in RAW264.7 cells enhanced viral titers. Furthermore, SLFN14 promoted the delay in viral NP translocation from cytoplasm to nucleus and enhanced RIG-I-mediated IFN-β signaling. In addition, SLFN14 overexpression promoted antiviral activity against varicella zoster virus (VZV), a DNA virus. In conclusion, our data suggest that SLFN14 is a novel antiviral factor for both DNA and RNA viruses.
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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.