Protein reactivity of 3,4-dihydroxyphenylacetaldehyde, a toxic dopamine metabolite, is dependent on both the aldehyde and the catechol.
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Monoamine oxidase B prompts mitochondrial and cardiac dysfunction in pressure overloaded heartsCatecholamine autotoxicity. Implications for pharmacology and therapeutics of Parkinson disease and related disordersAldehyde Dehydrogenase 1 making molecular inroads into the differential vulnerability of nigrostriatal dopaminergic neuron subtypes in Parkinson's diseaseAldehyde dehydrogenase inhibition generates a reactive dopamine metabolite autotoxic to dopamine neuronsEfficient and biologically relevant consensus strategy for Parkinson's disease gene prioritization.Vesicular integrity in Parkinson's diseaseCellular localization of dieldrin and structure-activity relationship of dieldrin analogues in dopaminergic cellsFrom L-dopa to dihydroxyphenylacetaldehyde: a toxic biochemical pathway plays a vital physiological function in insectsToxic Dopamine Metabolite DOPAL Forms an Unexpected Dicatechol Pyrrole Adduct with Lysines of α-SynucleinAldehyde dehydrogenase 1 defines and protects a nigrostriatal dopaminergic neuron subpopulationDivalent metal ions enhance DOPAL-induced oligomerization of alpha-synuclein.The neurotoxicity of DOPAL: behavioral and stereological evidence for its role in Parkinson disease pathogenesis.Determinants of buildup of the toxic dopamine metabolite DOPAL in Parkinson's disease.Aldehyde dehydrogenase 1-positive nigrostriatal dopaminergic fibers exhibit distinct projection pattern and dopamine release dynamics at mouse dorsal striatum.Benomyl, aldehyde dehydrogenase, DOPAL, and the catecholaldehyde hypothesis for the pathogenesis of Parkinson's disease.Relative inhibitory potency of molinate and metabolites with aldehyde dehydrogenase 2: implications for the mechanism of enzyme inhibitionA vesicular sequestration to oxidative deamination shift in myocardial sympathetic nerves in Parkinson's disease.Inhibition and covalent modification of tyrosine hydroxylase by 3,4-dihydroxyphenylacetaldehyde, a toxic dopamine metabolite.Oxidation of 3,4-dihydroxyphenylacetaldehyde, a toxic dopaminergic metabolite, to a semiquinone radical and an ortho-quinone.Methylmercury impairs canonical dopamine metabolism in rat undifferentiated pheochromocytoma (PC12) cells by indirect inhibition of aldehyde dehydrogenase.Decreased vesicular storage and aldehyde dehydrogenase activity in multiple system atrophy.Deficient vesicular storage: A common theme in catecholaminergic neurodegeneration.Catechols in post-mortem brain of patients with Parkinson disease.Oligomerization and Membrane-binding Properties of Covalent Adducts Formed by the Interaction of α-Synuclein with the Toxic Dopamine Metabolite 3,4-Dihydroxyphenylacetaldehyde (DOPAL).Vesicular uptake blockade generates the toxic dopamine metabolite 3,4-dihydroxyphenylacetaldehyde in PC12 cells: relevance to the pathogenesis of Parkinson's disease.DOPAL is transmissible to and oligomerizes alpha-synuclein in human glial cells.Stress, allostatic load, catecholamines, and other neurotransmitters in neurodegenerative diseases.Concepts of scientific integrative medicine applied to the physiology and pathophysiology of catecholamine systems.Nitrative and oxidative stress in toxicology and disease.DOPAL derived alpha-synuclein oligomers impair synaptic vesicles physiological function.Stress, allostatic load, catecholamines, and other neurotransmitters in neurodegenerative diseasesAge-dependent dopamine transporter dysfunction and Serine129 phospho-α-synuclein overload in G2019S LRRK2 mice.Chemopreventative effects of tetrahydrocurcumin on human diseases.The vesicular monoamine transporter 2: an underexplored pharmacological target.Membrane transporters as mediators of synaptic dopamine dynamics: implications for disease.Non-cytochrome P450-mediated bioactivation and its toxicological relevance.Dopamine and Cu+/2+ can induce oligomerization of α-synuclein in the absence of oxygen: Two types of oligomerization mechanisms for α-synuclein and related cell toxicity studies.Catechol and aldehyde moieties of 3,4-dihydroxyphenylacetaldehyde contribute to tyrosine hydroxylase inhibition and neurotoxicity.Dopamine-derived biological reactive intermediates and protein modifications: Implications for Parkinson's disease.Antioxidant-Mediated Modulation of Protein Reactivity for 3,4-Dihydroxyphenylacetaldehyde, a Toxic Dopamine Metabolite.
P2860
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P2860
Protein reactivity of 3,4-dihydroxyphenylacetaldehyde, a toxic dopamine metabolite, is dependent on both the aldehyde and the catechol.
description
2009 nî lūn-bûn
@nan
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
2009年论文
@zh
2009年论文
@zh-cn
name
Protein reactivity of 3,4-dihy ...... the aldehyde and the catechol.
@en
type
label
Protein reactivity of 3,4-dihy ...... the aldehyde and the catechol.
@en
prefLabel
Protein reactivity of 3,4-dihy ...... the aldehyde and the catechol.
@en
P2093
P2860
P356
P1476
Protein reactivity of 3,4-dihy ...... the aldehyde and the catechol.
@en
P2093
Jennifer N Rees
Jonathan A Doorn
Laurie L Eckert
Virginia R Florang
P2860
P304
P356
10.1021/TX9000557
P577
2009-07-01T00:00:00Z