Extracellular ATP and the P2X7 receptor in astrocyte-mediated motor neuron death: implications for amyotrophic lateral sclerosis. - Wikidata - awgldk - TriplyDB

Extracellular ATP and the P2X7 receptor in astrocyte-mediated motor neuron death: implications for amyotrophic lateral sclerosis.

Extracellular ATP and the P2X7 receptor in astrocyte-mediated motor neuron death: implications for amyotrophic lateral sclerosis.

http://www.wikidata.org/entity/Q33980768

about

The role of the immune system in neurodegenerative disorders: Adaptive or maladaptive?Novel molecular biomarkers at the blood-brain barrier in ALS Microglia centered pathogenesis in ALS: insights in cell interconnectivity Neuronal and glial purinergic receptors functions in neuron development and brain disease Precision Medicine in Multiple Sclerosis: Future of PET Imaging of Inflammation and Reactive Astrocytes Effect of Lead (Pb) on Inflammatory Processes in the Brain Pathophysiology of astroglial purinergic signalling Expression of ecto-nucleoside triphosphate diphosphohydrolase1-3 (NTPDase1-3) by cortical astrocytes after exposure to pro-inflammatory factors in vitro Extensive dysregulations of oligodendrocytic and astrocytic connexins are associated with disease progression in an amyotrophic lateral sclerosis mouse model.Neuronal P2X7 receptor-induced reactive oxygen species production contributes to nociceptive behavior in mice Spinal cord pathology is ameliorated by P2X7 antagonism in a SOD1-mutant mouse model of amyotrophic lateral sclerosis Phenotypically aberrant astrocytes that promote motoneuron damage in a model of inherited amyotrophic lateral sclerosis Some aspects of purinergic signaling in the ventricular system of porcine brain Extracellular ATP Selectively Upregulates Ecto-Nucleoside Triphosphate Diphosphohydrolase 2 and Ecto-5'-Nucleotidase by Rat Cortical Astrocytes In Vitro.Anti-apoptotic Effects of Bone Marrow on Human Islets: A Preliminary Report.P2X7 receptor-induced death of motor neurons by a peroxynitrite/FAS-dependent pathway.Neuroimmunity dynamics and the development of therapeutic strategies for amyotrophic lateral sclerosis.Phenotypic transition of microglia into astrocyte-like cells associated with disease onset in a model of inherited ALS Motor neuron impairment mediated by a sumoylated fragment of the glial glutamate transporter EAAT2 P2X7 antagonism using Brilliant Blue G reduces body weight loss and prolongs survival in female SOD1G93A amyotrophic lateral sclerosis mice.Purinergic signalling at the plasma membrane: a multipurpose and multidirectional mode to deal with amyotrophic lateral sclerosis and multiple sclerosis.Microglia and neuronal cell death.Neurotransmitter signaling in the pathophysiology of microglia.Advances in cellular models to explore the pathophysiology of amyotrophic lateral sclerosis.Disease origin and progression in amyotrophic lateral sclerosis: an immunology perspective.P2X7 receptor-pannexin 1 interaction mediates extracellular alpha-synuclein-induced ATP release in neuroblastoma SH-SY5Y cells.Switching from astrocytic neuroprotection to neurodegeneration by cytokine stimulation.ATP-induced cellular stress and mitochondrial toxicity in cells expressing purinergic P2X7 receptor.Mitochondrial superoxide generation enhances P2X7R-mediated loss of cell surface CD62L on naive human CD4+ T lymphocytes.Flow Synthesis and Biological Studies of an Analgesic Adamantane Derivative That Inhibits P2X7-Evoked Glutamate Release.NTPDase and 5'-nucleotidase activities in synaptosomes of rabbits experimentally infected with BoHV-5.ATP-Induced IL-1β Specific Secretion: True Under Stringent Conditions.Role of Neuroinflammation in Amyotrophic Lateral Sclerosis: Cellular Mechanisms and Therapeutic Implications.Connexin 43 in astrocytes contributes to motor neuron toxicity in amyotrophic lateral sclerosis.Astrocyte plasticity revealed by adaptations to severe proteotoxic stress.Ablation of P2X7 receptor exacerbates gliosis and motoneuron death in the SOD1-G93A mouse model of amyotrophic lateral sclerosis.When too much ATP is a bad thing: a pivotal role for P2X7 receptors in motor neuron degeneration.Glycoursodeoxycholic acid reduces matrix metalloproteinase-9 and caspase-9 activation in a cellular model of superoxide dismutase-1 neurodegeneration.P2X7R antagonism after subfailure overstretch injury of blood vessels reverses vasomotor dysfunction and prevents apoptosis.Role and Therapeutic Potential of Astrocytes in Amyotrophic Lateral Sclerosis.

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P2860

Extracellular ATP and the P2X7 receptor in astrocyte-mediated motor neuron death: implications for amyotrophic lateral sclerosis.

http://www.wikidata.org/entity/Q33980768

description

2010 nî lūn-bûn

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2010 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2010 թվականի հունիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

Extracellular ATP and the P2X7 ...... amyotrophic lateral sclerosis.

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Extracellular ATP and the P2X7 ...... amyotrophic lateral sclerosis.

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type

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Extracellular ATP and the P2X7 ...... amyotrophic lateral sclerosis.

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Extracellular ATP and the P2X7 ...... amyotrophic lateral sclerosis.

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Extracellular ATP and the P2X7 ...... amyotrophic lateral sclerosis.

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Extracellular ATP and the P2X7 ...... amyotrophic lateral sclerosis.

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Journal of Neuroinflammation

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Extracellular ATP and the P2X7 ...... amyotrophic lateral sclerosis

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Joseph S Beckman

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Luis Barbeito

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Mandi Gandelman

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Patricia Cassina

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P2860

Aggregation and Motor Neuron Toxicity of an ALS-Linked SOD1 Mutant Independent from Wild-Type SOD1

SOD1 mutations disrupt redox-sensitive Rac regulation of NADPH oxidase in a familial ALS model

Non-cell autonomous effect of glia on motor neurons in an embryonic stem cell-based ALS model

Systemic administration of an antagonist of the ATP-sensitive receptor P2X7 improves recovery after spinal cord injury

Primary glia expressing the G93A-SOD1 mutation present a neuroinflammatory phenotype and provide a cellular system for studies of glial inflammation

Molecular physiology of P2X receptors

Astrocytes expressing ALS-linked mutated SOD1 release factors selectively toxic to motor neurons

Abnormal excitatory amino acid metabolism in amyotrophic lateral sclerosis

Arginase 1 regulation of nitric oxide production is key to survival of trophic factor-deprived motor neurons

Unraveling the mechanisms involved in motor neuron degeneration in ALS

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amyotrophic lateral sclerosis

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