Drosophila Parkin requires PINK1 for mitochondrial translocation and ubiquitinates Mitofusin
Explore this paper's citation graph
Summary
It is shown in Drosophila cells that PINK1 is required to recruit Parkin to dysfunctional mitochondria and promote their degradation, and Mfn ubiquitination may provide a mechanism by which terminally damaged mitochondria are labeled and sequestered for degradation by autophagy.
- Type
- article
- Published
- 2010-03-01
- Cited by
- 755
- References
- 46
- Access
- Open access
- OpenAlex
- https://openalex.org/W1979645469
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:19150726
Keywords
Parkin, PINK1, Mitochondrial fission, Mitochondrion, Cell biology
References
- Visualization and quantification of mitochondrial dynamics in living animal cells.
- Does Impairment of the Ubiquitin-Proteasome System or the Autophagy-Lysosome Pathway Predispose Individuals to Neurodegenerative Disorders such as Parkinson's Disease?
- Mitochondrial fusion, fission and autophagy as a quality control axis: the bioenergetic view.
- Familial Parkinson disease gene product, parkin, is a ubiquitin-protein ligase
- The Parkinson's disease genes pink1 and parkin promote mitochondrial fission and/or inhibit fusion in Drosophila
- The PINK1/Parkin pathway regulates mitochondrial morphology
- Structural Basis of Mitochondrial Tethering by Mitofusin Complexes
- The kinase domain of mitochondrial PINK1 faces the cytoplasm
- Cytoplasmic Pink1 activity protects neurons from dopaminergic neurotoxin MPTP
- Diverse Effects of Pathogenic Mutations of Parkin That Catalyze Multiple Monoubiquitylation in Vitro*
- Positioning mitochondrial plasticity within cellular signaling cascades.
- The PINK1-Parkin pathway is involved in the regulation of mitochondrial remodeling process.
- PINK1 controls mitochondrial localization of Parkin through direct phosphorylation.
- A regulated interaction with the UIM protein Eps15 implicates parkin in EGF receptor trafficking and PI(3)K–Akt signalling
- Parkin mediates the degradation‐independent ubiquitination of Hsp70
- PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1
- The PINK1/Parkin pathway: a mitochondrial quality control system?
- Mitochondrial Alterations in PINK1 Deficient Cells Are Influenced by Calcineurin-Dependent Dephosphorylation of Dynamin-Related Protein 1
- Mitochondrial dysfunction in Drosophila PINK1 mutants is complemented by parkin
- Mitochondrial pathology and apoptotic muscle degeneration in Drosophila parkin mutants
Cited by
- An anticancer agent, pyrvinium pamoate inhibits the NADH-fumarate reductase system--a unique mitochondrial energy metabolism in tumour microenvironments.
- Analysis of neural subtypes reveals selective mitochondrial dysfunction in dopaminergic neurons from parkin mutants
- Parkin-catalyzed Ubiquitin-Ester Transfer Is Triggered by PINK1-dependent Phosphorylation*
- Mitochondria autophagy is induced after hypoxic/ischemic stress in a Drp1 dependent manner: the role of inhibition of Drp1 in ischemic brain damage.
- Parkin-induced ubiquitination of Mff promotes its association with p62/SQSTM1 during mitochondrial depolarization.
- Valosin-containing protein (VCP/p97) inhibitors relieve Mitofusin-dependent mitochondrial defects due to VCP disease mutants
- Maintaining mitochondria in beige adipose tissue
- What have we learned from Drosophila models of Parkinson's disease?
- Monitoring Mitophagy in Neuronal Cell Cultures
- Mitochondrial Dynamics: The Intersection of Form and Function
- Mitochondrial degradation and energy metabolism.
- Rôle de la dysfonction mitochondriale dans deux maladies neurodégénératives, la Maladie de Huntington et la Maladie de Parkinson
- Candidate genes for Parkinson disease: Lessons from pathogenesis.
- Molecular Mechanisms of Mitochondrial Transport in Neurons
- Analysis of mitochondrial quality control using a Drosophila model of Parkinson’s disease
- E2F1-dependent miR-421 regulates mitochondrial fragmentation and myocardial infarction by targeting Pink1
- Genetic mouse models of neurodegenerative diseases.
- Autophagy deregulation in neurodegenerative diseases – recent advances and future perspectives
- Parkin promotes the ubiquitination and degradation of the mitochondrial fusion factor mitofusin 1
- Transgenic nematodes as a model for Parkinson's disease
Related papers
- Induction of PINK1/Parkin-Mediated Mitophagy.
- Deciphering the Molecular Signals of PINK1/Parkin Mitophagy.
- Immunocytochemical Monitoring of PINK1/Parkin-Mediated Mitophagy in Cultured Cells.
- PINK1 Is Dispensable for Mitochondrial Recruitment of Parkin and Activation of Mitophagy in Cardiac Myocytes
- Commitment in the PINK1/Parkin mitophagy decision circuit
- Mitochondrial fission facilitates the selective mitophagy of protein aggregates
- The PINK1-Parkin pathway is involved in the regulation of mitochondrial remodeling process.
- The Parkinson's disease genes pink1 and parkin promote mitochondrial fission and/or inhibit fusion in Drosophila