ArticleCell2019
Regulation of HIV-1 Gag-Pol Expression by Shiftless, an Inhibitor of Programmed -1 Ribosomal Frameshifting.
Article in Cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 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.
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.
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Who cites it
94 citing papers in PubMed, 128 citations in OpenAlex.
- hnRNPC facilitates coronavirus replication by directly binding the frameshift-stimulatory element of viral genomic RNA.PLoS pathogens · 2026Article
- Coordinated translation initiation determines -1 programmed ribosomal frameshifting efficiency of chromosomal genes to impact on cell fitness.The FEBS journal · 2026Article
- Review
- Lost in translation: interferon-stimulated genes targeting flavivirus protein synthesis.Journal of virology · 2026Review
- An IRES-like cis-acting element located within the EV-A71 coding region drives translation independent of the 5'-IRES and modulates viral fitness through regulated binding of viral RNA to 3D polymerase.Journal of virology · 2026Article
- Positive-Strand RNA Viral RdRps: From Structure Conservation and Activity Assay to Drug Development.Molecules (Basel, Switzerland) · 2026Review
- Porcine reproductive and respiratory syndrome virus antagonizes the host restriction factor SHFL to sustain viral programmed ribosomal frameshifting and replication.Journal of virology · 2026Article
- ZFP36L2 is an interferon β -induced inhibitor that restricts the nuclear export of HIV-1 transcripts.Nature communications · 2026Article
- The anti-viral protein Shiftless blocks p-body formation during KSHV infection.The Journal of general virology · 2026Article
- Article
- Durable Management of Plant Viruses: Insights into Host Resistance and Tolerance Mechanisms.Biology · 2026Review
- Phosphorylation of Shiftless by casein kinase 1 δ/ε is required for its antiviral activity.Journal of virology · 2025Article
- Phosphorylation of shiftless is important for inhibiting the programmed -1 ribosomal frameshift.Science advances · 2025Article
- Human Schlafen 14 Cleavage of Short Double-Stranded RNAs Underpins its Antiviral Activity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A novel polypeptide encoded by circSPIRE1 promotes prostate cancer proliferation and migration by restraining the ubiquitin-dependent degradation of LRP5.Journal of experimental & clinical cancer research : CR · 2025Article
- Conformational Analysis and Structure-Altering Mutations of the HIV-1 Frameshifting Element.International journal of molecular sciences · 2025Article
- Stem loop binding protein promotes SARS-CoV-2 replication via -1 programmed ribosomal frameshifting.Signal transduction and targeted therapy · 2025Article
- Viral Strategies and Cellular Countermeasures That Regulate mRNA Access to the Translation Apparatus.Viruses · 2025Review
- Genetic variations of thePeerJ · 2025Article
- Imaging and Quantifying Ribosomal Frameshifting Dynamics with Single-RNA Precision in Live Cells.Methods in molecular biology (Clifton, N.J.) · 2025Article
34 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Programmed -1 ribosomal frameshifting (-1PRF) is a widely used translation recoding mechanism. HIV-1 expresses Gag-Pol protein from the Gag-coding mRNA through -1PRF, and the ratio of Gag to Gag-Pol is strictly maintained for efficient viral replication. Here, we report that the interferon-stimulated gene product C19orf66 (herein named Shiftless) is a host factor that inhibits the -1PRF of HIV-1. Shiftless (SFL) also inhibited the -1PRF of a variety of mRNAs from both viruses and cellular genes. SFL interacted with the -1PRF signal of target mRNA and translating ribosomes and caused premature translation termination at the frameshifting site. Downregulation of translation release factor eRF3 or eRF1 reduced SFL-mediated premature translation termination. We propose that SFL binding to target mRNA and the translating ribosome interferes with the frameshifting process. These findings identify SFL as a broad-spectrum inhibitor of -1PRF and help to further elucidate the mechanisms of -1PRF.
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What OpenQuestion holds
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.