ArticleMolecular cell2024
METTL17 is an Fe-S cluster checkpoint for mitochondrial translation.
Article in Molecular cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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Who cites it
33 citing papers in PubMed, 46 citations in OpenAlex.
- Integrative bioinformatics and machine learning reveal hub genes and immune signatures bridging type 2 diabetes mellitus, fracture susceptibility, and osteoblast differentiation dysfunction.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- METTL17 promotes gastric cancer progression via inhibiting glycogen synthase kinase-3β to activate Wnt/β-catenin signaling.Translational cancer research · 2026Article
- Review
- From Iron to Depression: The Crosstalk Between the Periphery and Brain.Neuroscience bulletin · 2026Review
- The iron-sulfur cluster assembly factor FDX2 is required for tumor initiation but not for growth of established tumors in transplantation models.The Journal of biological chemistry · 2026Article
- Mechanisms and disease relevance of mitochondrial translation in humans.Nature reviews. Molecular cell biology · 2026Review
- Iron-sulfur cofactors in nucleic acid metabolism and protein synthesis: Assembly, delivery, and putative roles in cellular and viral systems.The Journal of biological chemistry · 2026Review
- Exploring the mechanism of Dieda Qili Tablet on fracture healing based on network pharmacology combined with machine learning models.Scientific reports · 2026Article
- SIRT5-RNF126 coordinated regulation of METTL17 stability controls mitochondrial function and glioma progression.Cell & bioscience · 2026Article
- A kinetic mathematical model of comprehensive iron metabolism in a respiring yeast cell: a basic-pathways approach to solving a large system dynamically.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Article
- Translational activators align mRNAs at the small mitoribosomal subunit for translation initiation.Nature structural & molecular biology · 2026Article
- Integrative omics and experimental validation reveal METTL17 and SLC27A1 as biomarkers and potential therapeutic targets in chronic kidney disease.Frontiers in immunology · 2026Article
- Article
- The function of Mak16 in ribosome biogenesis depends on its [4Fe-4S] cluster.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mettl15-Mettl17 modulates the transition from early to late pre-mitoribosome.Structure (London, England : 1993) · 2025Article
- The methyltransferase-like proteins as core regulators of nucleic acid modifications and post-translation modification of proteins in disease pathogenesis and therapeutic implications.Biomarker research · 2025Review
- The proton motive force maintains mtDNA euploidy by balancing mtDNA replication with cell proliferation.bioRxiv : the preprint server for biology · 2025Article
- D-cysteine impairs tumour growth by inhibiting cysteine desulfurase NFS1.Nature metabolism · 2025Article
- The cytochrome oxidase defect in ISC-depleted yeast is caused by impaired iron-sulfur cluster maturation of the mitoribosome assembly factor Rsm22.FEBS letters · 2025Article
- Salutary Effects of Overexpression of Rsm22, an Assembly Factor for the Mitochondrial Ribosome, on Frataxin/Yfh1 Depletion Phenotypes inBiomolecules · 2025Article
Corrections and comments
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Authors and funding
12 authors at 8 institutions in 3 countries.
Funding
Abstract
Friedreich's ataxia (FA) is a debilitating, multisystemic disease caused by the depletion of frataxin (FXN), a mitochondrial iron-sulfur (Fe-S) cluster biogenesis factor. To understand the cellular pathogenesis of FA, we performed quantitative proteomics in FXN-deficient human cells. Nearly every annotated Fe-S cluster-containing protein was depleted, indicating that as a rule, cluster binding confers stability to Fe-S proteins. We also observed depletion of a small mitoribosomal assembly factor METTL17 and evidence of impaired mitochondrial translation. Using comparative sequence analysis, mutagenesis, biochemistry, and cryoelectron microscopy, we show that METTL17 binds to the mitoribosomal small subunit during late assembly and harbors a previously unrecognized [Fe
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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.