ArticleViruses2024
Schlafen14 Impairs HIV-1 Expression in a Codon Usage-Dependent Manner.
Article in Viruses, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 9 citations in OpenAlex.
- tRNA modifications in viral replication.The Journal of biological chemistry · 2026Review
- 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
- Evolutionary characterization of antiviral SAMD9/9L across kingdoms supports ancient convergence and lineage-specific adaptations.Nature ecology & evolution · 2025Article
- Human Schlafen 14 Cleavage of Short Double-Stranded RNAs Underpins its Antiviral Activity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- CryoEM structure of the SLFN14 endoribonuclease reveals insight into RNA binding and cleavage.Nature communications · 2025Article
- Ancient convergence with prokaryote defense and recent adaptations to lentiviruses in primates characterize the ancestral immune factors SAMD9s.bioRxiv : the preprint server for biology · 2025Article
- Structural and functional characterization of human SLFN14.Nucleic acids research · 2025Article
- Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Schlafen (SLFN) is a family of proteins upregulated by type I interferons with a regulatory role in translation. Intriguingly, SLFN14 associates with the ribosome and can degrade rRNA, tRNA, and mRNA in vitro, but a role in translation is still unknown. Ribosomes are important regulatory hubs during translation elongation of mRNAs rich in rare codons. Therefore, we evaluated the potential role of SLFN14 in the expression of mRNAs enriched in rare codons, using HIV-1 genes as a model. We found that, in a variety of cell types, including primary immune cells, SLFN14 regulates the expression of HIV-1 and non-viral genes based on their codon adaptation index, a measurement of the synonymous codon usage bias; consequently, SLFN14 inhibits the replication of HIV-1. The potent inhibitory effect of SLFN14 on the expression of the rare codon-rich transcript HIV-1 Gag was minimized by codon optimization. Mechanistically, we found that the endoribonuclease activity of SLFN14 is required, and that ribosomal RNA degradation is involved. Therefore, we propose that SLFN14 impairs the expression of HIV-1 transcripts rich in rare codons, in a catalytic-dependent manner.
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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.