ArticleNature2019
Mitochondrial protein translocation-associated degradation.
Article in Nature, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 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
160 citing papers in PubMed, 299 citations in OpenAlex.
- Cell-Type-Specific Calibration of Mitochondrial Ubiquitination in Stem Cell Fate Decisions.Stem cell reviews and reports · 2026Review
- Regulation of cellular proteostasis via mitochondrial protein import.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- Comparative analysis of Cdc48-dependent proteolysis at the ER, mitochondria and chloroplasts.Nature communications · 2026Review
- Redox signals and oxidative stress in the control of mitochondrial protein import.Protein science : a publication of the Protein Society · 2026Review
- Mass spectrometry proteomics for studying mitostasis.Protein science : a publication of the Protein Society · 2026Review
- The role of the nucleus in the control of mitochondrial precursor proteins in yeast.Protein science : a publication of the Protein Society · 2026Review
- Mitochondrial protein import stress causes lysosomal damage and progressive tissue atrophy.EMBO reports · 2026Article
- Rewiring Adipocyte Plasticity: The Redox-Mitochondrial Axis as a Driver of Beige Fat Immunometabolism and Adipose Inflammation.Biomolecules · 2026Review
- A dynamic gateway: Uncovering the expanded human TOM complex interactome and its regulatory complexity.Science advances · 2026Article
- Quality control of protein import into mammalian mitochondria.Protein science : a publication of the Protein Society · 2026Review
- Targeting prohibitins activates the ISR through DELE1-HRI by impairing protein import into the mitochondrial matrix.Cell death and differentiation · 2026Article
- mtHsp70 chaperone converts mitochondrial proteostasis stress into impaired protein import.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The integrated stress response suppresses PINK1-dependent mitophagy by preserving mitochondrial import efficiency.Nature communications · 2026Article
- Functions of J-domain proteins in mitochondrial protein biogenesis.Protein science : a publication of the Protein Society · 2026Review
- The endoplasmic reticulum in mitochondrial protein targeting: A neuronal perspective on organelle crosstalk.Protein science : a publication of the Protein Society · 2026Review
- Function and regulation of the mitochondrial stress response.Nature structural & molecular biology · 2026Review
- The role of ER-associated degradation and ER-phagy in health and disease.Signal transduction and targeted therapy · 2026Review
- Article
- The IQ-compete assay for measuring mitochondrial protein import efficiencies in living yeast cells.FEBS letters · 2026Article
- The many faces of p97/Cdc48 in mitochondrial homeostasis.Essays in biochemistry · 2025Review
100 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial biogenesis and functions depend on the import of precursor proteins via the 'translocase of the outer membrane' (TOM complex). Defects in protein import lead to an accumulation of mitochondrial precursor proteins that induces a range of cellular stress responses. However, constitutive quality-control mechanisms that clear trapped precursor proteins from the TOM channel under non-stress conditions have remained unknown. Here we report that in Saccharomyces cerevisiae Ubx2, which functions in endoplasmic reticulum-associated degradation, is crucial for this quality-control process. A pool of Ubx2 binds to the TOM complex to recruit the AAA ATPase Cdc48 for removal of arrested precursor proteins from the TOM channel. This mitochondrial protein translocation-associated degradation (mitoTAD) pathway continuously monitors the TOM complex under non-stress conditions to prevent clogging of the TOM channel with precursor proteins. The mitoTAD pathway ensures that mitochondria maintain their full protein-import capacity, and protects cells against proteotoxic stress induced by impaired transport of proteins into 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.