Parthanatos mediates AIMP2-activated age-dependent dopaminergic neuronal loss. - Wikidata - wikimedia - TriplyDB

Parthanatos mediates AIMP2-activated age-dependent dopaminergic neuronal loss.

Parthanatos mediates AIMP2-activated age-dependent dopaminergic neuronal loss.

http://www.wikidata.org/entity/Q30547326

about

Parkin structure and function Structure and function of the ARH family of ADP-ribosyl-acceptor hydrolases Poly (ADP-ribose) in the pathogenesis of Parkinson's disease Estrogen replacement therapy-induced neuroprotection against brain ischemia-reperfusion injury involves the activation of astrocytes via estrogen receptor β.Hydrocortisone-induced parkin prevents dopaminergic cell death via CREB pathway in Parkinson's disease model Transfer RNA and human disease Neuroprotectin D1 upregulates Iduna expression and provides protection in cellular uncompensated oxidative stress and in experimental ischemic stroke.VPS35 regulates parkin substrate AIMP2 toxicity by facilitating lysosomal clearance of AIMP2.Elovanoids are novel cell-specific lipid mediators necessary for neuroprotective signaling for photoreceptor cell integrity Neuroinflammation and neurodegeneration in adult rat brain from binge ethanol exposure: abrogation by docosahexaenoic acid.Poly(ADP-ribose) polymerase-dependent energy depletion occurs through inhibition of glycolysis.Interaction of NS2 with AIMP2 facilitates the switch from ubiquitination to SUMOylation of M1 in influenza A virus-infected cells.Genetic deficiency of the mitochondrial protein PGAM5 causes a Parkinson's-like movement disorder.Prevention of the degeneration of human dopaminergic neurons in an astrocyte co-culture system allowing endogenous drug metabolism YM155, a survivin suppressant, triggers PARP-dependent cell death (parthanatos) and inhibits esophageal squamous-cell carcinoma xenografts in mice Decoding Parkinson's Disease Pathogenesis: The Role of Deregulated mRNA Translation.Activation of tyrosine kinase c-Abl contributes to α-synuclein-induced neurodegeneration Adult Conditional Knockout of PGC-1α Leads to Loss of Dopamine Neurons.Enhancing NAD+ salvage metabolism is neuroprotective in a PINK1 model of Parkinson's disease.Overexpression of Parkinson's Disease-Associated Mutation LRRK2 G2019S in Mouse Forebrain Induces Behavioral Deficits and α-Synuclein Pathology Parkin and PINK1: much more than mitophagy Therapeutic strategies in Parkinson's disease: what we have learned from animal models.Nicotinamide Adenine Dinucleotide Metabolism and Neurodegeneration.Molecular changes in the postmortem parkinsonian brain.Opportunities for the repurposing of PARP inhibitors for the therapy of non-oncological diseases.The c-Abl inhibitor in Parkinson disease.The c-Abl inhibitor, nilotinib, protects dopaminergic neurons in a preclinical animal model of Parkinson's disease.Metabolic Dysfunction in Parkinson's Disease: Bioenergetics, Redox Homeostasis and Central Carbon Metabolism.PINK1 and Parkin are genetic modifiers for FUS-induced neurodegeneration.Trumping neurodegeneration: Targeting common pathways regulated by autosomal recessive Parkinson's disease genes.Ferroptosis: bug or feature?FAF1 mediates regulated necrosis through PARP1 activation upon oxidative stress leading to dopaminergic neurodegeneration Motor neuron death in ALS: programmed by astrocytes?Deficiency of Parkinson's disease-related gene Fbxo7 is associated with impaired mitochondrial metabolism by PARP activation.PARP-1 and p53 Regulate the Increased Susceptibility to Oxidative Death of Lymphocytes from MCI and AD Patients c-Abl and Parkinson's Disease: Mechanisms and Therapeutic Potential.CRISPR-Cas9 Mediated Telomere Removal Leads to Mitochondrial Stress and Protein Aggregation.Estrogen receptor activation contributes to RNF146 expression and neuroprotection in Parkinson's disease models.Synaptotagmin-11 is a critical mediator of parkin-linked neurotoxicity and Parkinson's disease-like pathology.α-Synuclein accumulation and GBA deficiency due to L444P GBA mutation contributes to MPTP-induced parkinsonism.

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P2860

Parthanatos mediates AIMP2-activated age-dependent dopaminergic neuronal loss.

http://www.wikidata.org/entity/Q30547326

description

2013 nî lūn-bûn

@nan

2013 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2013 թվականի օգոստոսին հրատարակված գիտական հոդված

@hy

2013年の論文

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2013年論文

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2013年論文

@zh-hant

2013年論文

@zh-hk

2013年論文

@zh-mo

2013年論文

@zh-tw

2013年论文

@wuu

name

Parthanatos mediates AIMP2-activated age-dependent dopaminergic neuronal loss.

@ast

Parthanatos mediates AIMP2-activated age-dependent dopaminergic neuronal loss.

@en

type

label

Parthanatos mediates AIMP2-activated age-dependent dopaminergic neuronal loss.

@ast

Parthanatos mediates AIMP2-activated age-dependent dopaminergic neuronal loss.

@en

prefLabel

Parthanatos mediates AIMP2-activated age-dependent dopaminergic neuronal loss.

@ast

Parthanatos mediates AIMP2-activated age-dependent dopaminergic neuronal loss.

@en

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Nature Neuroscience

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Parthanatos mediates AIMP2-activated age-dependent dopaminergic neuronal loss.

@en

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Byoung Dae Lee

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Debbie Swing

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Donghoon Kim

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Haisong Jiang

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Han Seok Ko

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Ho Chul Kang

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Joo-Ho Shin

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Lino Tessarollo

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Senthilkumar S Karuppagounder

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Sung-Ung Kang

http://www.w3.org/2001/XMLSchema#string

P2860

Missing pieces in the Parkinson's disease puzzle

PARIS (ZNF746) repression of PGC-1α contributes to neurodegeneration in Parkinson's disease

PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1

Phosphorylation by the c-Abl protein tyrosine kinase inhibits parkin's ubiquitination and protective function

Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism

Dopamine covalently modifies and functionally inactivates parkin

AIMP2/p38, the scaffold for the multi-tRNA synthetase complex, responds to genotoxic stresses via p53

Identification of far upstream element-binding protein-1 as an authentic Parkin substrate

S-nitrosylation of parkin regulates ubiquitination and compromises parkin's protective function

'Rejuvenation' protects neurons in mouse models of Parkinson's disease

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