ArticleCell reports2020
Mitochondria-Associated Degradation Pathway (MAD) Function beyond the Outer Membrane.
Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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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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
31 citing papers in PubMed, 48 citations in OpenAlex.
- Comparative analysis of Cdc48-dependent proteolysis at the ER, mitochondria and chloroplasts.Nature communications · 2026Review
- The transcription factor ANAC017 links mitochondrial retrograde signaling with the ubiquitin-proteasome system to control mitochondrial function in Arabidopsis.Plant communications · 2026Article
- Retrograde signaling is required for Slm35-mediated negative regulation of mitophagy in yeast.Biology open · 2026Article
- The many faces of p97/Cdc48 in mitochondrial homeostasis.Essays in biochemistry · 2025Review
- Navigating the landscape of protein folding and proteostasis: from molecular chaperones to therapeutic innovations.Signal transduction and targeted therapy · 2025Review
- Ubiquitin-mediated degradation restricts spatiotemporal accumulation of the cytoplasmic male sterility protein WA352 to anthers in rice.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Proteostasis and protein quality control in chloroplasts: mechanisms and novel insights related to protein mislocalization.Journal of experimental botany · 2025Review
- Tom40 functions as a channel for protein retrotranslocation in the mitochondria-associated degradation (MAD) pathway.Communications biology · 2025Article
- The impact of ERCell death & disease · 2025Article
- Mitochondria-targeted oligomeric α-synuclein induces TOM40 degradation and mitochondrial dysfunction in Parkinson's disease and parkinsonism-dementia of Guam.Cell death & disease · 2024Article
- Reply: Does the polyubiquitination pathway operate inside intact chloroplasts to remove proteins?The Plant cell · 2024Article
- Mitochondrial Quality Control Processes at the Crossroads of Cell Death and Survival: Mechanisms and Signaling Pathways.International journal of molecular sciences · 2024Review
- Mitochondria-Targeted Oligomeric α-Synuclein Induces TOM40 Degradation and Mitochondrial Dysfunction in Parkinson's Disease and Parkinsonism-Dementia of Guam.Research square · 2024Article
- Article
- Analysis of the mitochondria-associated degradation pathway (MAD) in yeast cells.Methods in enzymology · 2024Article
- Isolation of yeast mitochondria by affinity purification using magnetic beads.Methods in enzymology · 2024Article
- Chloroplast protein translocation pathways and ubiquitin-dependent regulation at a glance.Journal of cell science · 2023Article
- Imaging of mtHyPer7, a Ratiometric Biosensor for Mitochondrial Peroxide, in Living Yeast Cells.Journal of visualized experiments : JoVE · 2023Article
- Molecular Determinants of Mitochondrial Shape and Function and Their Role in Glaucoma.Antioxidants & redox signaling · 2023Review
- From mitochondria to sarcopenia: role of 17β-estradiol and testosterone.Frontiers in endocrinology · 2023Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
The mitochondria-associated degradation pathway (MAD) mediates ubiquitination and degradation of mitochondrial outer membrane (MOM) proteins by the proteasome. We find that the MAD, but not other quality-control pathways including macroautophagy, mitophagy, or mitochondrial chaperones and proteases, is critical for yeast cellular fitness under conditions of paraquat (PQ)-induced oxidative stress in mitochondria. Specifically, inhibition of the MAD increases PQ-induced defects in growth and mitochondrial quality and decreases chronological lifespan. We use mass spectrometry analysis to identify possible MAD substrates as mitochondrial proteins that exhibit increased ubiquitination in response to PQ treatment and inhibition of the MAD. We identify candidate substrates in the mitochondrial matrix and inner membrane and confirm that two matrix proteins are MAD substrates. Our studies reveal a broader function for the MAD in mitochondrial protein surveillance beyond the MOM and a major role for the MAD in cellular and mitochondrial fitness in response to chronic, low-level oxidative stress in mitochondria.
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What OpenQuestion holds
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.