ArticleThe EMBO journal2010
A functional peptidyl-tRNA hydrolase, ICT1, has been recruited into the human mitochondrial ribosome.
Article in The EMBO journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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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
98 citing papers in PubMed, 193 citations in OpenAlex.
- Mitochondrial translation termination, recycling, reinitiation, and rescue for in-frame and out-of-frame contexts.Nature communications · 2026Article
- Mechanisms and disease relevance of mitochondrial translation in humans.Nature reviews. Molecular cell biology · 2026Review
- Differential expression of mitochondria-associated genes in clinical samples of Plasmodium falciparum showing severe manifestations.BMC genomics · 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
- Evaluating the feasibility of gene replacement strategies to treat MTRFR deficiency.Disease models & mechanisms · 2025Article
- Illuminating mitochondrial translation through mouse models.Human molecular genetics · 2024Review
- Decoding the Enigma: Translation Termination in Human Mitochondria.Human molecular genetics · 2024Review
- Mitochondrial protein synthesis quality control.Human molecular genetics · 2024Review
- MIF-Modulated Spinal Proteins Associated with Persistent Bladder Pain: A Proteomics Study.International journal of molecular sciences · 2024Article
- Mutation of the PEBP-like domain of the mitoribosomal MrpL35/mL38 protein results in production of nascent chains with impaired capacity to assemble into OXPHOS complexes.Molecular biology of the cell · 2023Article
- Alterations of lipid-mediated mitophagy result in aging-dependent sensorimotor defects.Aging cell · 2023Article
- 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
- Human mtRF1 terminates COX1 translation and its ablation induces mitochondrial ribosome-associated quality control.Nature communications · 2022Article
- Mammalian HEMK1 methylates glutamine residue of the GGQ motif of mitochondrial release factors.Scientific reports · 2022Article
- Bacterial Ribosome Rescue Systems.Microorganisms · 2022Review
- Maintaining mitochondrial ribosome function: The role of ribosome rescue and recycling factors.RNA biology · 2022Review
- Multifunctions of CRIF1 in cancers and mitochondrial dysfunction.Frontiers in oncology · 2022Review
38 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Bioinformatic analysis classifies the human protein encoded by immature colon carcinoma transcript-1 (ICT1) as one of a family of four putative mitochondrial translation release factors. However, this has not been supported by any experimental evidence. As only a single member of this family, mtRF1a, is required to terminate the synthesis of all 13 mitochondrially encoded polypeptides, the true physiological function of ICT1 was unclear. Here, we report that ICT1 is an essential mitochondrial protein, but unlike the other family members that are matrix-soluble, ICT1 has become an integral component of the human mitoribosome. Release-factor assays show that although ICT1 has retained its ribosome-dependent PTH activity, this is codon-independent; consistent with its loss of both domains that promote codon recognition in class-I release factors. Mutation of the GGQ domain common to ribosome-dependent PTHs causes a loss of activity in vitro and, crucially, a loss of cell viability, in vivo. We suggest that ICT1 may be essential for hydrolysis of prematurely terminated peptidyl-tRNA moieties in stalled mitoribosomes.
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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.