ArticleScientific reports2020
K63-linked ubiquitylation induces global sequestration of mitochondria.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- CYLD-mediated lysine63 deubiquitination regulates synaptic transmission and autophagy to mitigate age-related sequelae.Nature communications · 2026Article
- Proteasome inhibition enhances lysosome-mediated targeted protein degradation.Cell death & disease · 2026Article
- Spatial-Bioenergetic-Immune Axis in Type 2 Diabetes Mellitus-Associated Sarcopenia: A Review from Pathogenesis to Targeted Reconstruction.Journal of inflammation research · 2026Review
- Role of p62 nuclear condensates in regulating ubiquitin-mediated proteasomal degradation.Essays in biochemistry · 2025Review
- The role of cardiolipin in mitochondrial dynamics and quality control in neuronal ischemia/reperfusion injury.Cell death & disease · 2025Review
- The Lysine Deprotonation Mechanism in a Ubiquitin Conjugating Enzyme.The journal of physical chemistry. B · 2025Article
- Deubiquitinating Enzymes Regulate Skeletal Muscle Mitochondrial Quality Control and Insulin Sensitivity in Patients With Type 2 Diabetes.Journal of cachexia, sarcopenia and muscle · 2025Article
- Trafficking of K63-polyubiquitin-modified membrane proteins in a macroautophagy-independent pathway is linked to ATG9A.Molecular biology of the cell · 2025Article
- Gaining Insight into Mitochondrial Targeting: AUTAC-Biguanide as an Anticancer Agent.Molecules (Basel, Switzerland) · 2024Article
- Localized K63 ubiquitin signaling is regulated by VCP/p97 during oxidative stress.bioRxiv : the preprint server for biology · 2024Article
- PA2G4/EBP1 ubiquitination by PRKN/PARKIN promotes mitophagy protecting neuron death in cerebral ischemia.Autophagy · 2024Article
- Crosstalk between ubiquitination and translation in neurodevelopmental disorders.Frontiers in molecular neuroscience · 2024Review
- Fast friends - Ubiquitin-like modifiers as engineered fusion partners.Seminars in cell & developmental biology · 2022Review
- Manipulating autophagic degradation in human diseases: from mechanisms to interventions.Life medicine · 2022Review
- The role of K63-linked polyubiquitin in several types of autophagy.Biologia futura · 2022Review
- Miro proteins and their role in mitochondrial transfer in cancer and beyond.Frontiers in cell and developmental biology · 2022Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Even though K63-linked polyubiquitin chains do not target proteins for proteasomal degradation, they play nevertheless a complementary protective role in maintaining protein homeostasis by directing malfunctioning proteins and organelles to inclusion bodies or autophagosomes. A paradigm for this process is the sequestration and autophagic degradation of dysfunctional mitochondria. Although studies have shown that K63-ubiquitylation of mitochondrial proteins by the ubiquitin ligase Parkin is important in this process, it is presently not clear if this modification also suffices to initiate this cascade of events. To address this question, we have engineered the ubiquitin ligase ProxE3, which in an inducible manner synthesizes K63-linked ubiquitin chains on the surface of mitochondria. We found that the presence of K63-linked ubiquitin chains on mitochondria resulted in the recruitment of the ubiquitin adaptor p62 and induced a dramatic redistribution of mitochondria, which was reminiscent to the Parkin-facilitated sequestration in response to mitochondrial uncoupler. However, ProxE3 did not induce autophagic degradation of mitochondria. Our data show that K63-linked ubiquitin chains at the mitochondrial membrane are sufficient for the induction of mitochondrial sequestration, but not mitophagy, without the need of extrinsically inflicting mitochondrial dysfunction.
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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.