Physiological phenotype and vulnerability in Parkinson's disease - Wikidata - awgldk - TriplyDB

Physiological phenotype and vulnerability in Parkinson's disease

Physiological phenotype and vulnerability in Parkinson's disease

http://www.wikidata.org/entity/Q36065850

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Cell-permeable parkin proteins suppress Parkinson disease-associated phenotypes in cultured cells and animals Converging roles of ion channels, calcium, metabolic stress, and activity pattern of Substantia nigra dopaminergic neurons in health and Parkinson's disease Mitochondrial complex I deactivation is related to superoxide production in acute hypoxia.Mitochondrial oxidant stress in locus coeruleus is regulated by activity and nitric oxide synthase.Subpicomolar diphenyleneiodonium inhibits microglial NADPH oxidase with high specificity and shows great potential as a therapeutic agent for neurodegenerative diseases.Phospholipase A2 - nexus of aging, oxidative stress, neuronal excitability, and functional decline of the aging nervous system? Insights from a snail model system of neuronal aging and age-associated memory impairment Unaltered striatal dopamine release levels in young Parkin knockout, Pink1 knockout, DJ-1 knockout and LRRK2 R1441G transgenic mice.Coexistence of glutamatergic spine synapses and shaft synapses in substantia nigra dopamine neurons.Impairment of PARK14-dependent Ca(2+) signalling is a novel determinant of Parkinson's disease Small heat shock proteins mediate cell-autonomous and -nonautonomous protection in a Drosophila model for environmental-stress-induced degeneration.RISC in PD: the impact of microRNAs in Parkinson's disease cellular and molecular pathogenesis.The pathology roadmap in Parkinson disease.Calcium signaling in Parkinson's disease.Presence of Androgen Receptor Variant in Neuronal Lipid Rafts.PKA Phosphorylation of NCLX Reverses Mitochondrial Calcium Overload and Depolarization, Promoting Survival of PINK1-Deficient Dopaminergic Neurons Implications of cellular models of dopamine neurons for disease.Imaging Adenosine Triphosphate (ATP)Selective neuronal vulnerability in Parkinson disease.Calcium signaling and molecular mechanisms underlying neurodegenerative diseases.The role of Ca2+ signaling in Parkinson's disease.The Hyperpolarization-Activated Current Determines Synaptic Excitability, Calcium Activity and Specific Viability of Substantia Nigra Dopaminergic Neurons.Inhibition of L-Type Ca2+ Channels by TRPC1-STIM1 Complex Is Essential for the Protection of Dopaminergic Neurons.Hypoxia-inducible factors regulate human and rat cystathionine β-synthase gene expression.Balance between the proximal dendritic compartment and the soma determines spontaneous firing rate in midbrain dopamine neurons.Cav1.3 channels control D2-autoreceptor responses via NCS-1 in substantia nigra dopamine neurons Parkinson's disease is associated with altered expression of CaV1 channels and calcium-binding proteins.Rotenone and elevated extracellular potassium concentration induce cell-specific fibrillation of α-synuclein in axons of cholinergic enteric neurons in the guinea-pig ileum.Extending roGFP Emission via Förster-Type Resonance Energy Transfer Relay Enables Simultaneous Dual Compartment Ratiometric Redox Imaging in Live Cells.Synaptotagmin-11 is a critical mediator of parkin-linked neurotoxicity and Parkinson's disease-like pathology.Parkinson's Disease Is Not Simply a Prion Disorder.Parkinson's Disease, the Dopaminergic Neuron and Gammahydroxybutyrate.Calcium dynamics control K-ATP channel-mediated bursting in substantia nigra dopamine neurons: a combined experimental and modeling study.Calcium Channel Antagonists as Disease-Modifying Therapy for Parkinson's Disease: Therapeutic Rationale and Current Status.Expression of Iron Transporters and Pathological Hallmarks of Parkinson's and Alzheimer's Diseases in the Brain of Young, Adult, and Aged Rats.Calcium CaV1 channel subtype mRNA expression in Parkinson's disease examined by in situ hybridization.Microglia Response During Parkinson's Disease: Alpha-Synuclein Intervention

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P2860

Physiological phenotype and vulnerability in Parkinson's disease

http://www.wikidata.org/entity/Q36065850

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Physiological phenotype and vulnerability in Parkinson's disease

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Physiological phenotype and vulnerability in Parkinson's disease

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Physiological phenotype and vulnerability in Parkinson's disease

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Physiological phenotype and vulnerability in Parkinson's disease

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Physiological phenotype and vulnerability in Parkinson's disease

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Physiological phenotype and vulnerability in Parkinson's disease

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Cold Spring Harbor Perspectives in Medicine

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Physiological phenotype and vulnerability in Parkinson's disease

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D James Surmeier

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Jaime N Guzman

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Javier Sanchez

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Paul T Schumacker

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P2860

Intraneuronal dopamine-quinone synthesis: A review

Familial Parkinson disease gene product, parkin, is a ubiquitin-protein ligase

Ca2+ binding to alpha-synuclein regulates ligand binding and oligomerization

Premature ageing in mice expressing defective mitochondrial DNA polymerase

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

The homocysteine-inducible endoplasmic reticulum (ER) stress protein Herp counteracts mutant α-synuclein-induced ER stress via the homeostatic regulation of ER-resident calcium release channel proteins

A forty-kilodalton protein of the inner membrane is the mitochondrial calcium uniporter

How mitochondria produce reactive oxygen species

Is the oxidative stress theory of aging dead?

MAM: more than just a housekeeper

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Parkinson's disease

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