Parkinson phenotype in aged PINK1-deficient mice is accompanied by progressive mitochondrial dysfunction in absence of neurodegeneration.
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MUL1 acts in parallel to the PINK1/parkin pathway in regulating mitofusin and compensates for loss of PINK1/parkinMitofusin 1 and mitofusin 2 are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagyInactivation 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-1Parkinson's Disease: The Mitochondria-Iron LinkThe Role of Autophagy, Mitophagy and Lysosomal Functions in Modulating Bioenergetics and Survival in the Context of Redox and Proteotoxic Damage: Implications for Neurodegenerative DiseasesMitochondria: A Therapeutic Target for Parkinson's Disease?Using iPS Cells toward the Understanding of Parkinson's DiseaseGenetically engineered mouse models of Parkinson's diseasePrimary skin fibroblasts as a model of Parkinson's diseaseMitochondrial dynamics and mitophagy in Parkinson's disease: disordered cellular power plant becomes a big deal in a major movement disorderMitochondrial involvement in neurodegenerative diseasesPotentiation of neurotoxicity in double-mutant mice with Pink1 ablation and A53T-SNCA overexpression.Increased expression of the dopamine transporter leads to loss of dopamine neurons, oxidative stress and l-DOPA reversible motor deficits.Tissue- and cell-specific mitochondrial defect in Parkin-deficient miceParkinson's disease: animal models and dopaminergic cell vulnerabilityMitochondrial impairment increases FL-PINK1 levels by calcium-dependent gene expressionGene-environment interactions: key to unraveling the mystery of Parkinson's diseaseBioenergetic consequences of PINK1 mutations in Parkinson diseaseThe Parkinson's gene PINK1 regulates cell cycle progression and promotes cancer-associated phenotypesMitochondrial dynamics--fusion, fission, movement, and mitophagy--in neurodegenerative diseasesThe PINK1/Parkin pathway regulates mitochondrial dynamics and function in mammalian hippocampal and dopaminergic neurons.Animal models of Parkinson's disease: vertebrate geneticsHyperexcitable substantia nigra dopamine neurons in PINK1- and HtrA2/Omi-deficient mice.Pathway-specific dopaminergic deficits in a mouse model of Angelman syndromeMitochondrial permeability transition pore regulates Parkinson's disease development in mutant α-synuclein transgenic mice.Enteric neurons from Parkinson's disease patients display ex vivo aberrations in mitochondrial structure.Neuron-selective changes in RNA transcripts related to energy metabolism in toxic models of parkinsonism in rodents.Early hypersynchrony in juvenile PINK1(-)/(-) motor cortex is rescued by antidromic stimulationMechanisms of body weight fluctuations in Parkinson's disease.Blood RNA biomarkers in prodromal PARK4 and rapid eye movement sleep behavior disorder show role of complexin 1 loss for risk of Parkinson's disease.Increased mitochondrial calcium sensitivity and abnormal expression of innate immunity genes precede dopaminergic defects in Pink1-deficient mice.Behavioral phenotyping of mouse models of Parkinson's disease.Aging decreases L-type calcium channel currents and pacemaker firing fidelity in substantia nigra dopamine neurons.A pivotal role for PINK1 and autophagy in mitochondrial quality control: implications for Parkinson disease.Autophagy as a stress-response and quality-control mechanism: implications for cell injury and human diseaseAging and energetics' 'Top 40' future research opportunities 2010-2013.Loss of mitochondrial peptidase Clpp leads to infertility, hearing loss plus growth retardation via accumulation of CLPX, mtDNA and inflammatory factors.Genetic determinants at the interface of cancer and neurodegenerative disease.To eat or not to eat: neuronal metabolism, mitophagy, and Parkinson's disease.Transgenic animal models of neurodegeneration based on human genetic studies.
P2860
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P2860
Parkinson phenotype in aged PINK1-deficient mice is accompanied by progressive mitochondrial dysfunction in absence of neurodegeneration.
description
2009 nî lūn-bûn
@nan
2009 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
2009 թվականի հունիսին հրատարակված գիտական հոդված
@hy
2009年の論文
@ja
2009年論文
@yue
2009年論文
@zh-hant
2009年論文
@zh-hk
2009年論文
@zh-mo
2009年論文
@zh-tw
2009年论文
@wuu
name
Parkinson phenotype in aged PI ...... n absence of neurodegeneration
@nl
Parkinson phenotype in aged PI ...... absence of neurodegeneration.
@ast
Parkinson phenotype in aged PI ...... absence of neurodegeneration.
@en
type
label
Parkinson phenotype in aged PI ...... n absence of neurodegeneration
@nl
Parkinson phenotype in aged PI ...... absence of neurodegeneration.
@ast
Parkinson phenotype in aged PI ...... absence of neurodegeneration.
@en
prefLabel
Parkinson phenotype in aged PI ...... n absence of neurodegeneration
@nl
Parkinson phenotype in aged PI ...... absence of neurodegeneration.
@ast
Parkinson phenotype in aged PI ...... absence of neurodegeneration.
@en
P2093
P2860
P50
P3181
P1433
P1476
Parkinson phenotype in aged PI ...... absence of neurodegeneration.
@en
P2093
Alexander Kurz
Alexei P Kudin
Andreas S Reichert
Annabelle Zimmermann
Dirk Wenzel
Dorothea Becker
Filomena Ricciardi
Georg Auburger
Hans-Hermann Hoepken
P2860
P3181
P356
10.1371/JOURNAL.PONE.0005777
P407
P577
2009-06-03T00:00:00Z