ArticlePLoS pathogens2016
Non-human Primate Schlafen11 Inhibits Production of Both Host and Viral Proteins.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Multiple Inhibitory Factors Act in the Late Phase of HIV-1 Replication: a Systematic Review of the Literature.Microbiology and molecular biology reviews : MMBR · 2018Pooled it
- Learning from nature: HIV elite controllers as blueprints for a functional cure.Virology journal · 2025Review
- SLFN11 counteracts the RFWD3-PRIMPOL DNA damage tolerance axis to restrain gapped DNA synthesis in response to replication stress.Nature communications · 2025Article
- Recurrent Evolutionary Innovations in Rodent and Primate Schlafen Genes.Genome biology and evolution · 2025Article
- SLFN11 Restricts LINE-1 Mobility.Cells · 2025Article
- Adaptation of CD4 in gorillas and chimpanzees conveyed resistance to simian immunodeficiency viruses.eLife · 2025Article
- Phosphorylation-mediated conformational change regulates human SLFN11.Nature communications · 2024Article
- Translation Inhibition Mediated by Interferon-Stimulated Genes during Viral Infections.Viruses · 2024Review
- Review
- Article
- "Transfer" of power: The intersection of DNA virus infection and tRNA biology.Seminars in cell & developmental biology · 2023Review
- Structural and biochemical characterization of Schlafen11 N-terminal domain.Nucleic acids research · 2023Article
- Mechanistic understanding of human SLFN11.Nature communications · 2022Article
- Schlafens Can Put Viruses to Sleep.Viruses · 2022Review
- Human cytomegalovirus protein RL1 degrades the antiviral factor SLFN11 via recruitment of the CRL4 E3 ubiquitin ligase complex.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Review
- Nuku, a family of primate retrocopies derived from KU70.G3 (Bethesda, Md.) · 2021Article
- SLFN11 Inactivation Induces Proteotoxic Stress and Sensitizes Cancer Cells to Ubiquitin Activating Enzyme Inhibitor TAK-243.Cancer research · 2021Article
- Positive natural selection in primate genes of the type I interferon response.BMC ecology and evolution · 2021Article
- Comparative proteomics identifies Schlafen 5 (SLFN5) as a herpes simplex virus restriction factor that suppresses viral transcription.Nature microbiology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Schlafen11 (encoded by the SLFN11 gene) has been shown to inhibit the accumulation of HIV-1 proteins. We show that the SLFN11 gene is under positive selection in simian primates and is species-specific in its activity against HIV-1. The activity of human Schlafen11 is relatively weak compared to that of some other primate versions of this protein, with the versions encoded by chimpanzee, orangutan, gibbon, and marmoset being particularly potent inhibitors of HIV-1 protein production. Interestingly, we find that Schlafen11 is functional in the absence of infection and reduces protein production from certain non-viral (GFP) and even host (Vinculin and GAPDH) transcripts. This suggests that Schlafen11 may just generally block protein production from non-codon optimized transcripts. Because Schlafen11 is an interferon-stimulated gene with a broad ability to inhibit protein production from many host and viral transcripts, its role may be to create a general antiviral state in the cell. Interestingly, the strong inhibitors such as marmoset Schlafen11 consistently block protein production better than weak primate Schlafen11 proteins, regardless of the virus or host target being analyzed. Further, we show that the residues to which species-specific differences in Schlafen11 potency map are distinct from residues that have been targeted by positive selection. We speculate that the positive selection of SLFN11 could have been driven by a number of different factors, including interaction with one or more viral antagonists that have yet to be identified.
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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.