Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Mitochondrial pathology and apoptotic muscle degeneration in Drosophila parkin mutants.
Increased glutathione S-transferase activity rescues dopaminergic neuron loss in a Drosophila model of Parkinson's disease.
Parkin negatively regulates JNK pathway in the dopaminergic neurons of Drosophila.
The Drosophila parkin homologue is required for normal mitochondrial dynamics during spermiogenesis.
Drosophila melanogaster Parkin ubiquitinates peanut and septin1 as an E3 ubiquitin-protein ligase.
Drosophila overexpressing parkin R275W mutant exhibits dopaminergic neuron degeneration and mitochondrial abnormalities.
The PINK1/Parkin pathway regulates mitochondrial morphology.
Pink1 regulates mitochondrial dynamics through interaction with the fission/fusion machinery.
The Parkinson's disease genes pink1 and parkin promote mitochondrial fission and/or inhibit fusion in Drosophila.
PINK1 controls mitochondrial localization of Parkin through direct phosphorylation.
Loss of parkin or PINK1 function increases Drp1-dependent mitochondrial fragmentation.
Leucine-Rich Repeat Kinase 2 interacts with Parkin, DJ-1 and PINK-1 in a Drosophila melanogaster model of Parkinson's disease.
Drosophila parkin requires PINK1 for mitochondrial translocation and ubiquitinates mitofusin.
Extended lifespan of Drosophila parkin mutants through sequestration of redox-active metals and enhancement of anti-oxidative pathways.
Parkin suppresses c-Jun N-terminal kinase-induced cell death via transcriptional regulation in Drosophila.
Diminution of eIF4E activity suppresses parkin mutant phenotypes.
The parkin mutant phenotype in the fly is largely rescued by metal-responsive transcription factor (MTF-1).
The PINK1-Parkin pathway promotes both mitophagy and selective respiratory chain turnover in vivo.
A molecular explanation for the recessive nature of parkin-linked Parkinson's disease.
Mitochondrial contagion induced by Parkin deficiency in Drosophila hearts and its containment by suppressing mitofusin.
The deubiquitinase USP15 antagonizes Parkin-mediated mitochondrial ubiquitination and mitophagy.
MUL1 acts in parallel to the PINK1/parkin pathway in regulating mitofusin and compensates for loss of PINK1/parkin.
PINK1-mediated phosphorylation of Parkin boosts Parkin activity in Drosophila.
Optimization of wrMTrck to monitor Drosophila larval locomotor activity.
PINK1-dependent phosphorylation of PINK1 and Parkin is essential for mitochondrial quality control.
Drosophila PINK1 and parkin loss-of-function mutants display a range of non-motor Parkinson's disease phenotypes.
PINK1 Phosphorylates MIC60/Mitofilin to Control Structural Plasticity of Mitochondrial Crista Junctions.
Ari-1 Regulates Myonuclear Organization Together with Parkin and Is Associated with Aortic Aneurysms.
Decision between mitophagy and apoptosis by Parkin via VDAC1 ubiquitination.
PARIS induced defects in mitochondrial biogenesis drive dopamine neuron loss under conditions of parkin or PINK1 deficiency.
PINK1, Keap1, and Rtnl1 regulate selective clearance of endoplasmic reticulum during development.
Glutathione s-transferase omega 1 activity is sufficient to suppress neurodegeneration in a Drosophila model of Parkinson disease.
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park mutants have reduced F1F0-ATP synthase activity and assembly, partly restored by DmGSTO1 expression
"expression of DmGSTO1 partially restores the activity and assembly of the mitochondrial F(1)F(0)-ATP synthase in parkin mutants"
UniProt record Q7KTX7 (PRKN_DROME)
Manual literature synthesis for park
FlyBase gene description for park (DROME)