Suppressing aberrant GluN3A expression rescues synaptic and behavioral impairments in Huntington's disease models. - Wikidata - awgldk - TriplyDB

Suppressing aberrant GluN3A expression rescues synaptic and behavioral impairments in Huntington's disease models.

Suppressing aberrant GluN3A expression rescues synaptic and behavioral impairments in Huntington's disease models.

http://www.wikidata.org/entity/Q37607024

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Serine racemase: a key player in apoptosis and necrosis A Huntingtin-based peptide inhibitor of caspase-6 provides protection from mutant Huntingtin-induced motor and behavioral deficits.SorCS2-mediated NR2A trafficking regulates motor deficits in Huntington's disease F-BAR family proteins, emerging regulators for cell membrane dynamic changes-from structure to human diseases.The contribution of rare and common variants in 30 genes to risk nicotine dependence Preclinical and clinical investigations of mood stabilizers for Huntington's disease: what have we learned?Reversal of cellular phenotypes in neural cells derived from Huntington's disease monkey-induced pluripotent stem cells Differential Synaptic and Extrasynaptic Glutamate-Receptor Alterations in Striatal Medium-Sized Spiny Neurons of Aged YAC128 Huntington's Disease Mice.Allosteric activation of M4 muscarinic receptors improve behavioral and physiological alterations in early symptomatic YAC128 mice.A role for Kalirin-7 in corticostriatal synaptic dysfunction in Huntington's disease DARPP-32 interaction with adducin may mediate rapid environmental effects on striatal neurons Protons Potentiate GluN1/GluN3A Currents by Attenuating Their Desensitisation.A flexible polyglutamine hinge opens new doors for understanding huntingtin function GluN3A: an NMDA receptor subunit with exquisite properties and functions.Corticostriatal synaptic adaptations in Huntington's disease Huntington's Disease: Pathogenic Mechanisms and Therapeutic Targets.Developmental alterations in Huntington's disease neural cells and pharmacological rescue in cells and mice.Cognitive dysfunction in Huntington's disease: mechanisms and therapeutic strategies beyond BDNF.Huntington's Disease: Mechanisms of Pathogenesis and Therapeutic Strategies.Differential Effects of Pharmacologic and Genetic Modulation of NMDA Receptor Activity on HIV/gp120-Induced Neuronal Damage in an In Vivo Mouse Model.Residues in the GluN1 C-terminal domain control kinetics and pharmacology of GluN1/GluN3A N-methyl-d-aspartate receptors.Methamphetamine abuse impairs motor cortical plasticity and function.Neurotrophin receptor p75(NTR) mediates Huntington's disease-associated synaptic and memory dysfunction.Fingolimod (FTY720) enhances hippocampal synaptic plasticity and memory in Huntington's disease by preventing p75NTR up-regulation and astrocyte-mediated inflammation.Huntington's disease: easing the NMDAR traffic jam.Metabotropic glutamate receptor 5 knockout promotes motor and biochemical alterations in a mouse model of Huntington's disease.Early and progressive circadian abnormalities in Huntington's disease sheep are unmasked by social environment.Early pridopidine treatment improves behavioral and transcriptional deficits in YAC128 Huntington disease mice.The siRNA-mediated knockdown of GluN3A in 46C-derived neural stem cells affects mRNA expression levels of neural genes, including known iGluR interactors.Molecular insights into cortico-striatal miscommunications in Huntington's disease.Altering cortical input unmasks synaptic phenotypes in the YAC128 cortico-striatal co-culture model of Huntington disease.

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Suppressing aberrant GluN3A expression rescues synaptic and behavioral impairments in Huntington's disease models.

http://www.wikidata.org/entity/Q37607024

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 14 July 2013

@en

vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

@cs

name

Suppressing aberrant GluN3A ex ...... n Huntington's disease models.

@en

Suppressing aberrant GluN3A ex ...... n Huntington's disease models.

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type

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Suppressing aberrant GluN3A ex ...... n Huntington's disease models.

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Suppressing aberrant GluN3A ex ...... n Huntington's disease models.

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prefLabel

Suppressing aberrant GluN3A ex ...... n Huntington's disease models.

@en

Suppressing aberrant GluN3A ex ...... n Huntington's disease models.

@nl

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Nature Medicine

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Suppressing aberrant GluN3A ex ...... n Huntington's disease models.

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Albert Giralt

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

Donald C Lo

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

Isabel Pérez-Otaño

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Jesús Torres-Peraza

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John F Wesseling

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Jordi Alberch

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José Martínez-Hernández

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Linda S Kaltenbach

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Mahmoud A Pouladi

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

Masahiko Watanabe

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

P2860

Huntingtin interacting proteins are genetic modifiers of neurodegeneration

A protein interaction network links GIT1, an enhancer of huntingtin aggregation, to Huntington's disease

Huntingtin is a cytoplasmic protein associated with vesicles in human and rat brain neurons

RNA association and nucleocytoplasmic shuttling by ataxin-1

Syndapin I, a synaptic dynamin-binding protein that associates with the neural Wiskott-Aldrich syndrome protein

Assembly with the NR1 subunit is required for surface expression of NR3A-containing NMDA receptors

PACSIN 1 interacts with huntingtin and is absent from synaptic varicosities in presymptomatic Huntington's disease brains

Opposing effects of polyglutamine expansion on native protein complexes contribute to SCA1

Increased NMDA current and spine density in mice lacking the NMDA receptor subunit NR3A

Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death

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1030-1038

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scholarly article

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10.1038/NM.3246

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P433

8

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19

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Michael R. Hayden

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2013-07-14T00:00:00Z

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249321118

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1032575262

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23852340

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Huntington disease

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3936794

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