Late-onset motoneuron disease caused by a functionally modified AMPA receptor subunit. - Wikidata - awgldk - TriplyDB

Late-onset motoneuron disease caused by a functionally modified AMPA receptor subunit.

Late-onset motoneuron disease caused by a functionally modified AMPA receptor subunit.

http://www.wikidata.org/entity/Q33936956

about

Inhibitory synaptic regulation of motoneurons: a new target of disease mechanisms in amyotrophic lateral sclerosis.Adaptive gene regulation in the Striatum of RGS9-deficient mice Transcript diversification in the nervous system: a to I RNA editing in CNS function and disease development Amygdala size in amyotrophic lateral sclerosis without dementia: an in vivo study using MRI volumetry Glutamate transporters and the excitotoxic path to motor neuron degeneration in amyotrophic lateral sclerosis.BMAA--an unusual cyanobacterial neurotoxin.A-to-I RNA editing and human disease.Unravelling the enigma of selective vulnerability in neurodegeneration: motor neurons resistant to degeneration in ALS show distinct gene expression characteristics and decreased susceptibility to excitotoxicity.Exposure of neurons to excitotoxic levels of glutamate induces cleavage of the RNA editing enzyme, adenosine deaminase acting on RNA 2, and loss of GLUR2 editing.The essential role of AMPA receptor GluR2 subunit RNA editing in the normal and diseased brain Astrocytes regulate GluR2 expression in motor neurons and their vulnerability to excitotoxicity.Novel toxicity of the unedited GluR2 AMPA receptor subunit dependent on surface trafficking and increased Ca2+-permeability.AMPA Receptor Phosphorylation and Synaptic Colocalization on Motor Neurons Drive Maladaptive Plasticity below Complete Spinal Cord Injury.TNF-α triggers rapid membrane insertion of Ca(2+) permeable AMPA receptors into adult motor neurons and enhances their susceptibility to slow excitotoxic injury.Dynamic regulation of RNA editing of ion channels and receptors in the mammalian nervous system.TARP γ-7 selectively enhances synaptic expression of calcium-permeable AMPARs.Altered presymptomatic AMPA and cannabinoid receptor trafficking in motor neurons of ALS model mice: implications for excitotoxicity.Evidence-based drug treatment in amyotrophic lateral sclerosis and upcoming clinical trials.ADARs: allies or enemies? The importance of A-to-I RNA editing in human disease: from cancer to HIV-1.Ca permeable AMPA channels in diseases of the nervous system.Antisense oligonucleotide therapy for the treatment of C9ORF72 ALS/FTD diseases.Glutamate receptors localize postsynaptically at neuromuscular junctions in mice.Selective vulnerability of motoneuron and perturbed mitochondrial calcium homeostasis in amyotrophic lateral sclerosis: implications for motoneurons specific calcium dysregulation.Intrathecal infusion of a Ca(2+)-permeable AMPA channel blocker slows loss of both motor neurons and of the astrocyte glutamate transporter, GLT-1 in a mutant SOD1 rat model of ALS.Abnormal exocytotic release of glutamate in a mouse model of amyotrophic lateral sclerosis.GluR2 deficiency accelerates motor neuron degeneration in a mouse model of amyotrophic lateral sclerosis.C9ORF72 repeat expansion causes vulnerability of motor neurons to Ca2+-permeable AMPA receptor-mediated excitotoxicity.EAAT2 and the Molecular Signature of Amyotrophic Lateral Sclerosis.Ionic Homeostasis Maintenance in ALS: Focus on New Therapeutic Targets

P2860

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P2860

Late-onset motoneuron disease caused by a functionally modified AMPA receptor subunit.

http://www.wikidata.org/entity/Q33936956

description

2005 nî lūn-bûn

@nan

2005 թուականի Ապրիլին հրատարակուած գիտական յօդուած

@hyw

2005 թվականի ապրիլին հրատարակված գիտական հոդված

@hy

2005年の論文

@ja

2005年論文

@yue

2005年論文

@zh-hant

2005年論文

@zh-hk

2005年論文

@zh-mo

2005年論文

@zh-tw

2005年论文

@wuu

name

Late-onset motoneuron disease caused by a functionally modified AMPA receptor subunit.

@ast

Late-onset motoneuron disease caused by a functionally modified AMPA receptor subunit.

@en

type

label

Late-onset motoneuron disease caused by a functionally modified AMPA receptor subunit.

@ast

Late-onset motoneuron disease caused by a functionally modified AMPA receptor subunit.

@en

prefLabel

Late-onset motoneuron disease caused by a functionally modified AMPA receptor subunit.

@ast

Late-onset motoneuron disease caused by a functionally modified AMPA receptor subunit.

@en

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PNAS.0501316102

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Proceedings of the National Academy of Sciences of the United States of America

P1476

Late-onset motoneuron disease caused by a functionally modified AMPA receptor subunit.

@en

P2093

Anthony J Groom

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

Bettina Hartmann

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Chrysanthy Ikonomidou

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Gerald Müller

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Hans-Christian Kornau

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Iris Bresink

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Karsten Tschauner

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Lechoslaw Turski

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Rohini Kuner

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Stefan Waibel

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P2860

Glutamate receptors: RNA editing and death of motor neurons

Glutamate carboxypeptidase II inhibition protects motor neurons from death in familial amyotrophic lateral sclerosis models

Central nervous system control of food intake

Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation

Unraveling the mechanisms involved in motor neuron degeneration in ALS

Amyotrophic lateral sclerosis

Point mutation in an AMPA receptor gene rescues lethality in mice deficient in the RNA-editing enzyme ADAR2

Sporadic amyotrophic lateral sclerosis with circumscribed temporal atrophy: a report of an autopsy case without dementia and with ubiquitinated intraneuronal inclusions.

Brain lesions in an infant rhesus monkey treated with monsodium glutamate.

The sinister side of Italian soccer.

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5826-5831

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scholarly article

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16

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102

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Peter H. Seeburg

Albert C Ludolph

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7910128

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15827116

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556301

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