Absence of nigral degeneration in aged parkin/DJ-1/PINK1 triple knockout mice. - Wikidata - awgldk - TriplyDB

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

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

http://www.wikidata.org/entity/Q41867056

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MUL1 acts in parallel to the PINK1/parkin pathway in regulating mitofusin and compensates for loss of PINK1/parkin Parkin-dependent degradation of the F-box protein Fbw7β promotes neuronal survival in response to oxidative stress by stabilizing Mcl-1 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 Mouse Genetic Models of Human Brain Disorders Evaluation of Models of Parkinson's Disease Induced pluripotent stem cells in Parkinson's disease: scientific and clinical challenges Mouse models of Parkinson's disease associated with mitochondrial dysfunction Genetically engineered mouse models of Parkinson's disease Mitochondrial dynamics and mitophagy in Parkinson's disease: disordered cellular power plant becomes a big deal in a major movement disorder Potentiation of neurotoxicity in double-mutant mice with Pink1 ablation and A53T-SNCA overexpression.Endogenous Parkin Preserves Dopaminergic Substantia Nigral Neurons following Mitochondrial DNA Mutagenic Stress A53T-alpha-synuclein overexpression impairs dopamine signaling and striatal synaptic plasticity in old mice Parkinson's disease: animal models and dopaminergic cell vulnerability Neuronal Mitophagy in Neurodegenerative Diseases Animal models of Parkinson's disease: vertebrate genetics Behavioral and neurotransmitter abnormalities in mice deficient for Parkin, DJ-1 and superoxide dismutase.Intrastriatal injection of α-synuclein can lead to widespread synucleinopathy independent of neuroanatomic connectivity.Genetic mutations linked to Parkinson's disease differentially control nucleolar activity in pre-symptomatic mouse models DJ-1 deficient mice demonstrate similar vulnerability to pathogenic Ala53Thr human alpha-syn toxicity.Parkinson's disease: insights from pathways.Parkin in the regulation of fat uptake and mitochondrial biology: emerging links in the pathophysiology of Parkinson's disease.Targeting mitochondrial dysfunction: role for PINK1 and Parkin in mitochondrial quality control.Unaltered striatal dopamine release levels in young Parkin knockout, Pink1 knockout, DJ-1 knockout and LRRK2 R1441G transgenic mice.Parkin is a lipid-responsive regulator of fat uptake in mice and mutant human cells.Early exposure to paraquat sensitizes dopaminergic neurons to subsequent silencing of PINK1 gene expression in mice.Animal models of Parkinson's disease: a source of novel treatments and clues to the cause of the disease.Mitochondrial dysfunction in genetic animal models of Parkinson's disease Mitochondrial dynamics and Parkinson's disease: focus on parkin.Loss of leucine-rich repeat kinase 2 causes age-dependent bi-phasic alterations of the autophagy pathway The Polg Mutator Phenotype Does Not Cause Dopaminergic Neurodegeneration in DJ-1-Deficient Mice.Mitochondria: the next (neurode)generation Parkinsonism due to mutations in PINK1, parkin, and DJ-1 and oxidative stress and mitochondrial pathways.BAG2 Gene-mediated Regulation of PINK1 Protein Is Critical for Mitochondrial Translocation of PARKIN and Neuronal Survival Drosophila as a model to study mitochondrial dysfunction in Parkinson's disease.One-step generation of triple gene-targeted pigs using CRISPR/Cas9 system The roles of PINK1, parkin, and mitochondrial fidelity in Parkinson's disease PINK1 deficiency attenuates astrocyte proliferation through mitochondrial dysfunction, reduced AKT and increased p38 MAPK activation, and downregulation of EGFR.Autophagy and human diseases.Surprising behavioral and neurochemical enhancements in mice with combined mutations linked to Parkinson's disease.Changes in functional organization and white matter integrity in the connectome in Parkinson's disease.

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P2860

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

http://www.wikidata.org/entity/Q41867056

description

2009 nî lūn-bûn

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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2009年论文

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2009年论文

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name

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

@en

type

label

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

@en

prefLabel

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

@en

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J.1471-4159.2009.06350.X

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Journal of Neurochemistry

P1476

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

@en

P2093

Clement A Gautier

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Jie Shen

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Tohru Kitada

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Youren Tong

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P2860

Down regulation of DJ-1 enhances cell death by oxidative stress, ER stress, and proteasome inhibition

Mitochondrial localization of the Parkinson's disease related protein DJ-1: implications for pathogenesis

DJ-1 has a role in antioxidative stress to prevent cell death

Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism

Association of PINK1 and DJ-1 confers digenic inheritance of early-onset Parkinson's disease

Mutations in the DJ-1 gene associated with autosomal recessive early-onset parkinsonism

PINK1 is necessary for long term survival and mitochondrial function in human dopaminergic neurons

Mitochondrial localization of DJ-1 leads to enhanced neuroprotection

Hereditary early-onset Parkinson's disease caused by mutations in PINK1

Clinical features and neuroimaging of PARK7-linked parkinsonism

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