Clinically approved heterocyclics act on a mitochondrial target and reduce stroke-induced pathology. - Wikidata - awgldk - TriplyDB

Clinically approved heterocyclics act on a mitochondrial target and reduce stroke-induced pathology.

Clinically approved heterocyclics act on a mitochondrial target and reduce stroke-induced pathology.

http://www.wikidata.org/entity/Q33204952

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Evaluation of Dimebon in cellular model of Huntington's disease Therapeutic neuroprotective agents for amyotrophic lateral sclerosis Dietary macronutrients modulate the fatty acyl composition of rat liver mitochondrial cardiolipins Inhibitors of cytochrome c release with therapeutic potential for Huntington's disease High throughput screening for neurodegeneration and complex disease phenotypes.Mitochondrial dysfunction in the limelight of Parkinson's disease pathogenesis.Disturbed Ca2+ signaling and apoptosis of medium spiny neurons in Huntington's disease.Dipyrone inhibits neuronal cell death and diminishes hypoxic/ischemic brain injury Finding promiscuous old drugs for new uses.Identification of specific pluripotent stem cell death--inducing small molecules by chemical screening.Autophagy induction enhances TDP43 turnover and survival in neuronal ALS models.Reactive gamma-ketoaldehydes formed via the isoprostane pathway disrupt mitochondrial respiration and calcium homeostasis.A cell-based fascin bioassay identifies compounds with potential anti-metastasis or cognition-enhancing functions.Of mice and men: modelling post-stroke depression experimentally.Redundant cell death mechanisms as relics and backups.The Mitochondrial Permeability Transition Pore: Channel Formation by F-ATP Synthase, Integration in Signal Transduction, and Role in Pathophysiology.Dietary Omega-3 Fatty Acids Do Not Change Resistance of Rat Brain or Liver Mitochondria to Ca(2+) and/or Prooxidants.Promethazine protects against 3-nitropropionic acid-induced neurotoxicity.The mitochondrial permeability transition in neurologic disease Qualitative Characterization of the Rat Liver Mitochondrial Lipidome using LC-MS Profiling and High Energy Collisional Dissociation (HCD) All Ion Fragmentation.Methazolamide and melatonin inhibit mitochondrial cytochrome C release and are neuroprotective in experimental models of ischemic injury Differential susceptibility to excitotoxic stress in YAC128 mouse models of Huntington disease between initiation and progression of disease Inhibition of mitochondrial membrane permeability as a putative pharmacological target for cardioprotection.Mitochondrial proteomics as a selective tool for unraveling Parkinson's disease pathogenesis.New drug targets in depression: inflammatory, cell-mediated immune, oxidative and nitrosative stress, mitochondrial, antioxidant, and neuroprogressive pathways. And new drug candidates--Nrf2 activators and GSK-3 inhibitors.Impaired mitochondrial function in psychiatric disorders.Mitochondria and the central nervous system: searching for a pathophysiological basis of psychiatric disorders.Phenothiazines Enhance Mild Hypothermia-induced Neuroprotection via PI3K/Akt Regulation in Experimental Stroke.Qualitative characterization of the rat liver mitochondrial lipidome using all ion fragmentation on an Exactive benchtop Orbitrap MS.Separation of cis-trans phospholipid isomers using reversed phase LC with high resolution MS detection.Lipidomics profiling by high-resolution LC-MS and high-energy collisional dissociation fragmentation: focus on characterization of mitochondrial cardiolipins and monolysocardiolipins.Nortriptyline protects mitochondria and reduces cerebral ischemia/hypoxia injury.Kinetic model for Ca2+-induced permeability transition in energized liver mitochondria discriminates between inhibitor mechanisms.Systematic Identification of MCU Modulators by Orthogonal Interspecies Chemical Screening.Zinc irreversibly damages major enzymes of energy production and antioxidant defense prior to mitochondrial permeability transition.Neuroprotective Effect of Nortriptyline in Overt Hepatic Encephalopathy Through Attenuation of Mitochondrial Dysfunction

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P2860

Clinically approved heterocyclics act on a mitochondrial target and reduce stroke-induced pathology.

http://www.wikidata.org/entity/Q33204952

description

2004 nî lūn-bûn

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2004 թուականի Յուլիսին հրատարակուած գիտական յօդուած

@hyw

2004 թվականի հուլիսին հրատարակված գիտական հոդված

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2004年の論文

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2004年論文

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2004年論文

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2004年論文

@zh-hk

2004年論文

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2004年論文

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2004年论文

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name

Clinically approved heterocycl ...... duce stroke-induced pathology.

@ast

Clinically approved heterocycl ...... duce stroke-induced pathology.

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type

label

Clinically approved heterocycl ...... duce stroke-induced pathology.

@ast

Clinically approved heterocycl ...... duce stroke-induced pathology.

@en

prefLabel

Clinically approved heterocycl ...... duce stroke-induced pathology.

@ast

Clinically approved heterocycl ...... duce stroke-induced pathology.

@en

P1433

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P2860

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Journal of Experimental Medicine

P1476

Clinically approved heterocycl ...... educe stroke-induced pathology

@en

P2093

Abraham M Brown

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Bruce S Kristal

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

Irina G Stavrovskaya

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Jill Heemskerk

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

John P Blass

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

M Flint Beal

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

Malini V Narayanan

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

Robert M Friedlander

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S Stanley Young

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

Wenhua Zhang

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P2860

The HIV-1 viral protein R induces apoptosis via a direct effect on the mitochondrial permeability transition pore

The central executioner of apoptosis: multiple connections between protease activation and mitochondria in Fas/APO-1/CD95- and ceramide-induced apoptosis

Mechanisms of p75-mediated death of hippocampal neurons. Role of caspases.

Mitochondrial permeability transition in acute neurodegeneration

Spreading depression and focal brain ischemia induce cyclooxygenase-2 in cortical neurons through N-methyl-D-aspartic acid-receptors and phospholipase A2

Mitochondrial calcium transport: physiological and pathological relevance

Mitochondrial dysfunction is a primary event in glutamate neurotoxicity

Mitochondria and apoptosis

Bid, Bax, and lipids cooperate to form supramolecular openings in the outer mitochondrial membrane

The calmodulin antagonist trifluoperazine in transient focal brain ischemia in rats. Anti-ischemic effect and therapeutic window.

P304

211-222

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scholarly article

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10.1084/JEM.20032053

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2

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200

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Boris Krasnikov

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2004-07-01T00:00:00Z

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8446600

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15263028

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2212009

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