ArticlePLoS genetics2016
Human Cells Require Non-stop Ribosome Rescue Activity in Mitochondria.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 41 citations in OpenAlex.
- Blocked transcription-translation complexes are rescued by transcript release followed byJournal of bacteriology · 2026Article
- Ribosomal protein bL27 protects translating ribosomes from tmRNA-SmpB.Science advances · 2026Article
- Mitochondrial translation termination, recycling, reinitiation, and rescue for in-frame and out-of-frame contexts.Nature communications · 2026Article
- Ribosomal Protein bL27 Protects Translating Ribosomes from tmRNA-SmpB.bioRxiv : the preprint server for biology · 2026Article
- Plant MutS2 proteins function in plastid ribosome quality control.bioRxiv : the preprint server for biology · 2025Article
- Knockout of the mitoribosome rescue factors Ict1 or Mtrfr is viable in zebrafish but not mice: compensatory mechanisms underlying each factor's loss.FEBS open bio · 2025Article
- Emerging mechanisms of human mitochondrial translation regulation.Trends in biochemical sciences · 2025Review
- Article
- RqcH supports survival in the absence of non-stop ribosome rescue factors.bioRxiv : the preprint server for biology · 2024Article
- Illuminating mitochondrial translation through mouse models.Human molecular genetics · 2024Review
- Mitochondrial protein synthesis quality control.Human molecular genetics · 2024Review
- Translation in Mitochondrial Ribosomes.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Nonstop mRNAs generate a ground state of mitochondrial gene expression noise.Science advances · 2022Article
- Ribosome collisions: New ways to initiate ribosome rescue.Current biology : CB · 2022Article
- Maintaining mitochondrial ribosome function: The role of ribosome rescue and recycling factors.RNA biology · 2022Review
- Diversity and Similarity of Termination and Ribosome Rescue in Bacterial, Mitochondrial, and Cytoplasmic Translation.Biochemistry. Biokhimiia · 2021Review
- Mechanisms and regulation of protein synthesis in mitochondria.Nature reviews. Molecular cell biology · 2021Review
- A stalled-ribosome rescue factor Pth3 is required for mitochondrial translation against antibiotics in Saccharomyces cerevisiae.Communications biology · 2021Article
- Functional Diversity of Mitochondrial Peptidyl-tRNA Hydrolase ICT1 in Human Cells.Frontiers in molecular biosciences · 2021Review
- Ribosome Rescue Pathways in Bacteria.Frontiers in microbiology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Bacteria use trans-translation and the alternative rescue factors ArfA (P36675) and ArfB (Q9A8Y3) to hydrolyze peptidyl-tRNA on ribosomes that stall near the 3' end of an mRNA during protein synthesis. The eukaryotic protein ICT1 (Q14197) is homologous to ArfB. In vitro ribosome rescue assays of human ICT1 and Caulobacter crescentus ArfB showed that these proteins have the same activity and substrate specificity. Both ArfB and ICT1 hydrolyze peptidyl-tRNA on nonstop ribosomes or ribosomes stalled with ≤6 nucleotides extending past the A site, but are unable to hydrolyze peptidyl-tRNA when the mRNA extends ≥14 nucleotides past the A site. ICT1 provided sufficient ribosome rescue activity to support viability in C. crescentus cells that lacked both trans-translation and ArfB. Likewise, expression of ArfB protected human cells from death when ICT1 was silenced with siRNA. These data indicate that ArfB and ICT1 are functionally interchangeable, and demonstrate that ICT1 is a ribosome rescue factor. Because ICT1 is essential in human cells, these results suggest that ribosome rescue activity in mitochondria is required in humans.
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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.