The parkinsonian neurotoxin MPP+ opens the mitochondrial permeability transition pore and releases cytochrome c in isolated mitochondria via an oxidative mechanism.
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Inhibition of excessive mitochondrial fission reduced aberrant autophagy and neuronal damage caused by LRRK2 G2019S mutationMitochondria as a therapeutic target in heart failureMitochondria as a target for neurotoxins and neuroprotective agentsVanadium induces dopaminergic neurotoxicity via protein kinase Cdelta dependent oxidative signaling mechanisms: relevance to etiopathogenesis of Parkinson's diseaseAcute and/or chronic stress models modulate CuZnSOD and MnSOD protein expression in rat liverInteraction among mitochondria, mitogen-activated protein kinases, and nuclear factor-kappaB in cellular models of Parkinson's disease.Neurotoxic Abeta peptides increase oxidative stress in vivo through NMDA-receptor and nitric-oxide-synthase mechanisms, and inhibit complex IV activity and induce a mitochondrial permeability transition in vitro.Inhibition by R(+) or S(-) pramipexole of caspase activation and cell death induced by methylpyridinium ion or beta amyloid peptide in SH-SY5Y neuroblastoma.Interactions among nitric oxide and Bcl-family proteins after MPP+ exposure of SH-SY5Y neural cells I: MPP+ increases mitochondrial NO and Bax protein.MPP+ induces the endoplasmic reticulum stress response in rabbit brain involving activation of the ATF-6 and NF-kappaB signaling pathways.Ammonia induces the mitochondrial permeability transition in primary cultures of rat astrocytes.Pharmacological properties of BN82451: a novel multitargeting neuroprotective agent.Cell type-specific gene expression of midbrain dopaminergic neurons reveals molecules involved in their vulnerability and protectionEffect of heme iron valence state on the conformation of cytochrome c and its association with membrane interfaces. A CD and EPR investigation.Apoptotic mode of cell death in substantia nigra following intranigral infusion of the parkinsonian neurotoxin, MPP+ in Sprague-Dawley rats: cellular, molecular and ultrastructural evidences.Mitochondrial quality control: insights on how Parkinson's disease related genes PINK1, parkin, and Omi/HtrA2 interact to maintain mitochondrial homeostasis.Mitochondria targeted peptides protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity.Mitochondrial dysfunction in the limelight of Parkinson's disease pathogenesis.An AAV-derived Apaf-1 dominant negative inhibitor prevents MPTP toxicity as antiapoptotic gene therapy for Parkinson's disease.Development of mitochondria-targeted aromatic-cationic peptides for neurodegenerative diseases.Complex I deficiency primes Bax-dependent neuronal apoptosis through mitochondrial oxidative damageLoss of DJ-1 does not affect mitochondrial respiration but increases ROS production and mitochondrial permeability transition pore openingProtein kinase D1 (PKD1) phosphorylation promotes dopaminergic neuronal survival during 6-OHDA-induced oxidative stress.Distinct mPTP activation mechanisms in ischaemia-reperfusion: contributions of Ca2+, ROS, pH, and inorganic polyphosphate.Paeonolum protects against MPP(+)-induced neurotoxicity in zebrafish and PC12 cells.Neuroprotective effects of α-melanocyte-stimulating hormone against the neurotoxicity of 1-methyl-4-phenylpyridinium.Normal cellular prion protein protects against manganese-induced oxidative stress and apoptotic cell death.Pharmacological inhibition of neuronal NADPH oxidase protects against 1-methyl-4-phenylpyridinium (MPP+)-induced oxidative stress and apoptosis in mesencephalic dopaminergic neuronal cellsMicroRNA-7 Regulates the Function of Mitochondrial Permeability Transition Pore by Targeting VDAC1 Expression.The mitochondrial permeability transition in neurologic diseaseMolecular pathways of programmed cell death in experimental Parkinson's disease.Near-infrared light via light-emitting diode treatment is therapeutic against rotenone- and 1-methyl-4-phenylpyridinium ion-induced neurotoxicity.Mitochondria as targets for chemotherapy.The Short Isoform of DNAJB6 Protects against 1-Methyl-4-phenylpridinium Ion-Induced Apoptosis in LN18 Cells via Inhibiting Both ROS Formation and Mitochondrial Membrane Potential Loss.MPTP mouse models of Parkinson's disease: an update.Beyond muscles: The untapped potential of creatine.Rasagiline and selegiline suppress calcium efflux from mitochondria by PK11195-induced opening of mitochondrial permeability transition pore: a novel anti-apoptotic function for neuroprotection.Pinocembrin protects SH-SY5Y cells against MPP+-induced neurotoxicity through the mitochondrial apoptotic pathway.Studies on black tea (Camellia sinensis) extract as a potential antioxidant and a probable radioprotector.Astragaloside IV prevents MPP⁺-induced SH-SY5Y cell death via the inhibition of Bax-mediated pathways and ROS production.
P2860
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P2860
The parkinsonian neurotoxin MPP+ opens the mitochondrial permeability transition pore and releases cytochrome c in isolated mitochondria via an oxidative mechanism.
description
1999 nî lūn-bûn
@nan
1999 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի հունվարին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
The parkinsonian neurotoxin MP ...... ia via an oxidative mechanism.
@ast
The parkinsonian neurotoxin MP ...... ia via an oxidative mechanism.
@en
type
label
The parkinsonian neurotoxin MP ...... ia via an oxidative mechanism.
@ast
The parkinsonian neurotoxin MP ...... ia via an oxidative mechanism.
@en
prefLabel
The parkinsonian neurotoxin MP ...... ia via an oxidative mechanism.
@ast
The parkinsonian neurotoxin MP ...... ia via an oxidative mechanism.
@en
P2093
P1476
The parkinsonian neurotoxin MP ...... ria via an oxidative mechanism
@en
P2093
J P Bennett
W D Parker
P356
10.1016/S0925-4439(98)00083-0
P407
P577
1999-01-01T00:00:00Z