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Title
The mitochondrial kinase PINK1: functions beyond mitophagy
Authors
Keywords
-
Journal
JOURNAL OF NEUROCHEMISTRY
Volume 139, Issue -, Pages 232-239
Publisher
Wiley
Online
2016-06-02
DOI
10.1111/jnc.13655
References
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Related references
Note: Only part of the references are listed.- PINK1 activation–turning on a promiscuous kinase
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- PINK1 phosphorylates ubiquitin to activate Parkin E3 ubiquitin ligase activity
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- PINK1 is degraded through the N-end rule pathway
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- TRAP1 rescues PINK1 loss-of-function phenotypes
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- High-content genome-wide RNAi screens identify regulators of parkin upstream of mitophagy
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- PINK1-Phosphorylated Mitofusin 2 Is a Parkin Receptor for Culling Damaged Mitochondria
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- Drosophila Trap1 protects against mitochondrial dysfunction in a PINK1/parkin model of Parkinson’s disease
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- Role of PINK1 Binding to the TOM Complex and Alternate Intracellular Membranes in Recruitment and Activation of the E3 Ligase Parkin
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- Mitochondrial processing peptidase regulates PINK1 processing, import and Parkin recruitment
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- Inactivation ofPink1Genein VivoSensitizes Dopamine-producing Neurons to 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and Can Be Rescued by Autosomal Recessive Parkinson Disease Genes,ParkinorDJ-1
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- Regulation of mitochondrial permeability transition pore by PINK1
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- Vitamin K2 Is a Mitochondrial Electron Carrier That Rescues Pink1 Deficiency
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- PINK1 autophosphorylation upon membrane potential dissipation is essential for Parkin recruitment to damaged mitochondria
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- PINK1-mediated phosphorylation of the Parkin ubiquitin-like domain primes mitochondrial translocation of Parkin and regulates mitophagy
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- PINK1 is activated by mitochondrial membrane potential depolarization and stimulates Parkin E3 ligase activity by phosphorylating Serine 65
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- The Yeast Complex I Equivalent NADH Dehydrogenase Rescues pink1 Mutants
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- PINK1 and Parkin Target Miro for Phosphorylation and Degradation to Arrest Mitochondrial Motility
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- Functional alteration of PARL contributes to mitochondrial dysregulation in Parkinson's disease
- (2011) Guang Shi et al. HUMAN MOLECULAR GENETICS
- Depletion of PINK1 affects mitochondrial metabolism, calcium homeostasis and energy maintenance
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- The mitochondrial intramembrane protease PARL cleaves human Pink1 to regulate Pink1 trafficking
- (2011) Cathrin Meissner et al. JOURNAL OF NEUROCHEMISTRY
- Bioenergetic Consequences of PINK1 Mutations in Parkinson Disease
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- Pink1 regulates the oxidative phosphorylation machinery via mitochondrial fission
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- PINK1 cleavage at position A103 by the mitochondrial protease PARL
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- Perturbations in Mitochondrial Dynamics Induced by Human Mutant PINK1 Can Be Rescued by the Mitochondrial Division Inhibitor mdivi-1
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- Mitochondrial membrane potential regulates PINK1 import and proteolytic destabilization by PARL
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- (2010) Sven Geisler et al. NATURE CELL BIOLOGY
- Mitochondrial membrane potential decrease caused by loss of PINK1 is not due to proton leak, but to respiratory chain defects
- (2010) Taku Amo et al. NEUROBIOLOGY OF DISEASE
- Enhanced vulnerability of PARK6 patient skin fibroblasts to apoptosis induced by proteasomal stress
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- PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin
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- Pink1 Forms a Multiprotein Complex with Miro and Milton, Linking Pink1 Function to Mitochondrial Trafficking†
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- Parkinson's disease mutations in PINK1 result in decreased Complex I activity and deficient synaptic function
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- Differential effects of PINK1 nonsense and missense mutations on mitochondrial function and morphology
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- Loss of Parkin or PINK1 Function Increases Drp1-dependent Mitochondrial Fragmentation
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- Loss of PINK1 Function Promotes Mitophagy through Effects on Oxidative Stress and Mitochondrial Fission
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- PINK1-Associated Parkinson's Disease Is Caused by Neuronal Vulnerability to Calcium-Induced Cell Death
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- Silencing of PINK1 Expression Affects Mitochondrial DNA and Oxidative Phosphorylation in DOPAMINERGIC Cells
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- Mitochondrial Alterations in PINK1 Deficient Cells Are Influenced by Calcineurin-Dependent Dephosphorylation of Dynamin-Related Protein 1
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- Parkinson Phenotype in Aged PINK1-Deficient Mice Is Accompanied by Progressive Mitochondrial Dysfunction in Absence of Neurodegeneration
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- Rhomboid-7 and HtrA2/Omi act in a common pathway with the Parkinson's disease factors Pink1 and Parkin
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- Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
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- Biochemical aspects of the neuroprotective mechanism of PTEN-induced kinase-1 (PINK1)
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- Mitochondrial Respiratory Dysfunction in Familiar Parkinsonism Associated with PINK1 Mutation
- (2008) Claudia Piccoli et al. NEUROCHEMICAL RESEARCH
- Cytoplasmic Pink1 activity protects neurons from dopaminergic neurotoxin MPTP
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- Loss of PINK1 causes mitochondrial functional defects and increased sensitivity to oxidative stress
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- Pink1 regulates mitochondrial dynamics through interaction with the fission/fusion machinery
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- The PINK1/Parkin pathway regulates mitochondrial morphology
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- The Parkinson's disease genes pink1 and parkin promote mitochondrial fission and/or inhibit fusion in Drosophila
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