ArticleNature communications2018
Quantitative proteomics identifies redox switches for global translation modulation by mitochondrially produced reactive oxygen species.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers.
What it found
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The trial behind it
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Who cites it
129 citing papers in PubMed, 240 citations in OpenAlex.
- L-Glutamine Supplementation Improves the Benefits of Combined-Exercise Training on Oral Redox Balance and Inflammatory Status in Elderly Individuals.Oxidative medicine and cellular longevity · 2020Trial
- Ageing alters cysteine oxidation-regulated redox signalling in skeletal muscle: Integrative omics and AI-based structural predictions.Experimental physiology · 2026Article
- Mass spectrometry proteomics for studying mitostasis.Protein science : a publication of the Protein Society · 2026Review
- Redox signals and oxidative stress in the control of mitochondrial protein import.Protein science : a publication of the Protein Society · 2026Review
- Integrated analysis of the redoxome and zinc proteome links ribosomal protein oxidation to zinc homeostasis.Redox biology · 2026Article
- Perturbation of mitochondrial CaStress biology · 2026Article
- Identification and analysis of oxidative stress-related genes associated with the occurrence and development of diabetic retinopathy.Scientific reports · 2026Article
- Trans-kingdom coupling of redox signaling to environmental cell stress responses through multiphase partitioning.bioRxiv : the preprint server for biology · 2026Article
- A Post-GWAS Analysis of the Shared Genetic Architecture Between COVID-19 and Coronary Artery Disease.International journal of molecular sciences · 2026Article
- RNA binding proteinScience advances · 2026Article
- AQP7 Protects Vitrified Sheep GV-Stage Oocyte Maturation via Mitochondrial Activity.Animals : an open access journal from MDPI · 2026Article
- Leigh Syndrome Pathomechanism Involves Region-Specific Innate Immune Activation in Ndufs4 Knockout Mice.Cellular and molecular neurobiology · 2026Article
- Stress-induced mitochondrial fragmentation in endothelial cells disrupts blood-retinal barrier integrity causing neurodegeneration.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- ARG2 drives osteoblast senescence by repressing mitophagy via the IκB-NF-κB-TXN2 signaling axis: implications for age-associated osteoporosis.Theranostics · 2026Article
- A niche-dependent redox rheostat regulates epithelial stem cell fate.Nature communications · 2025Article
- From Electron Imbalance to Network Collapse: Decoding the Redox Code of Ischemic Stroke for Biomarker-Guided Precision Neuroprotection.International journal of molecular sciences · 2025Review
- Mitochondrial complex III-derived ROS amplify immunometabolic changes in astrocytes and promote dementia pathology.Nature metabolism · 2025Article
- Translational regulation in stress biology.Nature cell biology · 2025Review
- Celastrol inhibits the DPYSL2-JAK/STAT pathway by targeting mito-IDHs mediated mitochondrial metabolism to exhaust breast cancer.Acta pharmacologica Sinica · 2025Article
- A Review of Methionine and Cysteine: Their Roles as Sinks for Reactive Oxygen and Nitrogen Species, Including Bioinformatic Analysis of Their Percent Compositions in Metabolic Proteins.Indian journal of clinical biochemistry : IJCB · 2025Review
69 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
The generation of reactive oxygen species (ROS) is inevitably linked to life. However, the precise role of ROS in signalling and specific targets is largely unknown. We perform a global proteomic analysis to delineate the yeast redoxome to a depth of more than 4,300 unique cysteine residues in over 2,200 proteins. Mapping of redox-active thiols in proteins exposed to exogenous or endogenous mitochondria-derived oxidative stress reveals ROS-sensitive sites in several components of the translation apparatus. Mitochondria are the major source of cellular ROS. We demonstrate that increased levels of intracellular ROS caused by dysfunctional mitochondria serve as a signal to attenuate global protein synthesis. Hence, we propose a universal mechanism that controls protein synthesis by inducing reversible changes in the translation machinery upon modulating the redox status of proteins involved in translation. This crosstalk between mitochondria and protein synthesis may have an important contribution to pathologies caused by dysfunctional mitochondria.
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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.