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Loss of PINK1 causes mitochondrial functional defects and increased sensitivity to oxidative stress

Proceedings of the National Academy of Sciences - PNAS, 2008-08, Vol.105 (32), p.11364-11369

2008

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Absence of nigral degeneration in aged parkin/DJ-1/PINK1 triple knockout mice

Journal of neurochemistry, 2009-11, Vol.111 (3), p.696-702

2009

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History of Parkinson's Disease-Associated Gene, Parkin : Research over a Quarter Century in Quest of Finding the Physiological Substrate

International journal of molecular sciences, 2023-12, Vol.24 (23), p.16734

2023

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Ellagic Acid Prevents α-Synuclein Aggregation and Protects SH-SY5Y Cells from Aggregated α-Synuclein-Induced Toxicity via Suppression of Apoptosis and Activation of Autophagy

International journal of molecular sciences, 2021-12, Vol.22 (24), p.13398

2021

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Loss of DJ-1 does not affect mitochondrial respiration but increases ROS production and mitochondrial permeability transition pore opening

PloS one, 2012-07, Vol.7 (7), p.e40501-e40501

2012

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Parkin Precipitates on Mitochondria via Aggregation and Autoubiquitination

International journal of molecular sciences, 2023-05, Vol.24 (10), p.9027

2023

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Ellagic Acid Prevents Dopamine Neuron Degeneration from Oxidative Stress and Neuroinflammation in MPTP Model of Parkinson's Disease

Biomolecules (Basel, Switzerland), 2020-11, Vol.10 (11), p.1519

2020

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Impaired dopamine release and synaptic plasticity in the striatum of PINK1-deficient mice

Proceedings of the National Academy of Sciences - PNAS, 2007-07, Vol.104 (27), p.11441-11446

2007

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Ellagic Acid Prevents α-Synuclein Spread and Mitigates Toxicity by Enhancing Autophagic Flux in an Animal Model of Parkinson's Disease

Nutrients, 2023-12, Vol.16 (1), p.85

2023

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Cytoplasmic Pink1 activity protects neurons from dopaminergic neurotoxin MPTP

Proceedings of the National Academy of Sciences - PNAS, 2008-02, Vol.105 (5), p.1716-1721

2008

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Nigrostriatal Dopaminergic Deficits and Hypokinesia Caused by Inactivation of the Familial Parkinsonism-Linked Gene DJ-1

Neuron (Cambridge, Mass.), 2005-02, Vol.45 (4), p.489-496

2005

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Impaired dopamine release and synaptic plasticity in the striatum of Parkin-/- mice

Journal of neurochemistry, 2009-07, Vol.110 (2), p.613-621

2009

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Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism

Nature (London), 1998-04, Vol.392 (6676), p.605-608

1998

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Immunohistochemical and subcellular localization of parkin protein: Absence of protein in autosomal recessive juvenile parkinsonism patients

Annals of neurology, 1999-05, Vol.45 (5), p.668-672

1999

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Brain region specific mitophagy capacity could contribute to selective neuronal vulnerability in Parkinson's disease

Proteome science, 2011-09, Vol.9 (1), p.59-59, Article 59

2011

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History of Parkinson’s Disease-Associated Gene, IParkin/I: Research over a Quarter Century in Quest of Finding the Physiological Substrate

International journal of molecular sciences, 2023-11, Vol.24 (23)

2023

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Expression of PINK1 in the brain, eye and ear of mouse during embryonic development

Journal of chemical neuroanatomy, 2011-03, Vol.41 (2), p.73-85

2011

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Mitophagy-dependent necroptosis contributes to the pathogenesis of COPD

The Journal of clinical investigation, 2014-09, Vol.124 (9), p.3987-4003

2014

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Dose-related biphasic effect of the Parkinson’s disease neurotoxin MPTP, on the spread, accumulation, and toxicity of α-synuclein

Neurotoxicology (Park Forest South), 2021-05, Vol.84, p.41-52

2021

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PINK1 controls mitochondrial localization of Parkin through direct phosphorylation

Biochemical and biophysical research communications, 2008-12, Vol.377 (3), p.975-980

2008

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Molecular cloning, gene expression, and identification of a splicing variant of the mouse parkin gene

Mammalian genome, 2000-06, Vol.11 (6), p.417-421

2000

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Inactivation of Pink1 Gene in Vivo Sensitizes Dopamine-producing Neurons to 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and Can Be Rescued by Autosomal Recessive Parkinson Disease Genes, Parkin or DJ-1

The Journal of biological chemistry, 2012-06, Vol.287 (27), p.23162-23170

2012

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An Autopsy Case of Schilder’s Variant of Multiple Sclerosis (Schilder’s Disease)

European neurology, 2006-05, Vol.55 (2), p.103-107

2006

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A Microdeletion of D6S305 in a Family of Autosomal Recessive Juvenile Parkinsonism (PARK2)

Genomics (San Diego, Calif.), 1998-04, Vol.49 (1), p.143-146

1998

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Parkin reverses intracellular β-amyloid accumulation and its negative effects on proteasome function

Journal of neuroscience research, 2010-01, Vol.88 (1), p.167-178

2010

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Loss of PINK1 causes mitochondrial functional defects and increased sensitivity to oxidative stress

Absence of nigral degeneration in aged parkin/DJ-1/PINK1 triple knockout mice

History of Parkinson's Disease-Associated Gene, Parkin : Research over a Quarter Century in Quest of Finding the Physiological Substrate

Ellagic Acid Prevents α-Synuclein Aggregation and Protects SH-SY5Y Cells from Aggregated α-Synuclein-Induced Toxicity via Suppression of Apoptosis and Activation of Autophagy

Loss of DJ-1 does not affect mitochondrial respiration but increases ROS production and mitochondrial permeability transition pore opening

Parkin Precipitates on Mitochondria via Aggregation and Autoubiquitination

Ellagic Acid Prevents Dopamine Neuron Degeneration from Oxidative Stress and Neuroinflammation in MPTP Model of Parkinson's Disease

Impaired dopamine release and synaptic plasticity in the striatum of PINK1-deficient mice

Ellagic Acid Prevents α-Synuclein Spread and Mitigates Toxicity by Enhancing Autophagic Flux in an Animal Model of Parkinson's Disease

Cytoplasmic Pink1 activity protects neurons from dopaminergic neurotoxin MPTP

Nigrostriatal Dopaminergic Deficits and Hypokinesia Caused by Inactivation of the Familial Parkinsonism-Linked Gene DJ-1

Impaired dopamine release and synaptic plasticity in the striatum of Parkin-/- mice

Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism

Immunohistochemical and subcellular localization of parkin protein: Absence of protein in autosomal recessive juvenile parkinsonism patients

Brain region specific mitophagy capacity could contribute to selective neuronal vulnerability in Parkinson's disease

History of Parkinson’s Disease-Associated Gene, IParkin/I: Research over a Quarter Century in Quest of Finding the Physiological Substrate

Expression of PINK1 in the brain, eye and ear of mouse during embryonic development

Mitophagy-dependent necroptosis contributes to the pathogenesis of COPD

Dose-related biphasic effect of the Parkinson’s disease neurotoxin MPTP, on the spread, accumulation, and toxicity of α-synuclein

PINK1 controls mitochondrial localization of Parkin through direct phosphorylation

Molecular cloning, gene expression, and identification of a splicing variant of the mouse parkin gene

Inactivation of Pink1 Gene in Vivo Sensitizes Dopamine-producing Neurons to 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and Can Be Rescued by Autosomal Recessive Parkinson Disease Genes, Parkin or DJ-1

An Autopsy Case of Schilder’s Variant of Multiple Sclerosis (Schilder’s Disease)

A Microdeletion of D6S305 in a Family of Autosomal Recessive Juvenile Parkinsonism (PARK2)

Parkin reverses intracellular β-amyloid accumulation and its negative effects on proteasome function

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