ArticleMolecular cell2021
Mitochondrial-derived compartments facilitate cellular adaptation to amino acid stress.
Article in Molecular cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 70 citations in OpenAlex.
- Elevation of HNeuroscience bulletin · 2026Article
- Mitochondrially tethered Mmm1 can function as a sole lipid transporter at ER-mitochondria contacts.The Journal of cell biology · 2026Article
- Mitochondrial-derived compartments buffer outer membrane protein load during acute mitochondrial adaptation.bioRxiv : the preprint server for biology · 2026Article
- Vacuole pH loss triggers ESCRT-dependent plasma membrane remodeling to prevent amino acid toxicity.bioRxiv : the preprint server for biology · 2026Article
- Newcastle disease virus hijacks mitophagy to reprogram amino acid metabolism for enhanced replication.Autophagy · 2026Article
- Function and regulation of the mitochondrial stress response.Nature structural & molecular biology · 2026Review
- MISO regulates mitochondrial dynamics and mtDNA homeostasis by establishing membrane subdomains.Nature cell biology · 2026Article
- Mitochondria: from powerhouses of cells to hubs in antitumor immunity.Frontiers in immunology · 2026Review
- TIMP1 Derived from Mesenchymal Stem Cells Promotes Bladder Cancer Progression by Regulating the Formation of VDIMs through the RAP1 Pathway.International journal of biological sciences · 2026Article
- Intracellular Salmonella hijacks the mitochondrial citrate carrier to evade host oxidative defenses.Nature communications · 2025Article
- Leucine inhibits degradation of outer mitochondrial membrane proteins to adapt mitochondrial respiration.Nature cell biology · 2025Article
- L-Glutamate enables the EGFR-MEK-ERK-mTFB2 axis to enhance mitochondrial biogenesis in intestinal stem cells.Stem cell research & therapy · 2025Article
- Sensing within: Mitochondrial inside-out signal transduction.Cell chemical biology · 2025Review
- Alterations in lipid saturation trigger remodeling of the outer mitochondrial membrane.Molecular biology of the cell · 2025Article
- Ablation of LAT2 Transporter Causes Intramuscular Glutamine Accumulation and Inhibition of Fasting-Induced Proteolysis.Journal of cachexia, sarcopenia and muscle · 2025Article
- Molecular mechanisms of mitochondrial dynamics.Nature reviews. Molecular cell biology · 2025Review
- Privileged proteins with a second residence: dual targeting and conditional re-routing of mitochondrial proteins.The FEBS journal · 2024Review
- Mitochondrial-derived compartments remove surplus proteins from the outer mitochondrial membrane.The Journal of cell biology · 2024Article
- Mitochondrial-derived compartments are multilamellar domains that encase membrane cargo and cytosol.The Journal of cell biology · 2024Article
- Article
Corrections and comments
- Commented on by
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Amino acids are essential building blocks of life. However, increasing evidence suggests that elevated amino acids cause cellular toxicity associated with numerous metabolic disorders. How cells cope with elevated amino acids remains poorly understood. Here, we show that a previously identified cellular structure, the mitochondrial-derived compartment (MDC), functions to protect cells from amino acid stress. In response to amino acid elevation, MDCs are generated from mitochondria, where they selectively sequester and deplete SLC25A nutrient carriers and their associated import receptor Tom70 from the organelle. Generation of MDCs promotes amino acid catabolism, and their formation occurs simultaneously with transporter removal at the plasma membrane via the multivesicular body (MVB) pathway. The combined loss of vacuolar amino acid storage, MVBs, and MDCs renders cells sensitive to high amino acid stress. Thus, we propose that MDCs operate as part of a coordinated cell network that facilitates amino acid homeostasis through post-translational nutrient transporter remodeling.
Indexed as
Identifiers
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.