Suppression of neurodegeneration and increased neurotransmission caused by expanded full-length huntingtin accumulating in the cytoplasm - Wikidata - awgldk - TriplyDB

Suppression of neurodegeneration and increased neurotransmission caused by expanded full-length huntingtin accumulating in the cytoplasm

Suppression of neurodegeneration and increased neurotransmission caused by expanded full-length huntingtin accumulating in the cytoplasm

http://www.wikidata.org/entity/Q36514656

about

Huntingtin's function in axonal transport is conserved in Drosophila melanogaster Drosophila as an In Vivo Model for Human Neurodegenerative Disease The kynurenine pathway modulates neurodegeneration in a Drosophila model of Huntington's disease Systematic analysis of fly models with multiple drivers reveals different effects of ataxin-1 and huntingtin in neuron subtype-specific expression Delivery of GABAARs to synapses is mediated by HAP1-KIF5 and disrupted by mutant huntingtin.Amyloid oligomer neurotoxicity, calcium dysregulation, and lipid rafts In silico discovery and experimental validation of new protein-protein interactions A Drosophila model for TDP-43 proteinopathy.Drosophila melanogaster in the study of human neurodegeneration.Using membrane-targeted green fluorescent protein to monitor neurotoxic protein-dependent degeneration of Drosophila eyes Drosophila Models of Huntington's Disease exhibit sleep abnormalities Central regulation of locomotor behavior of Drosophila melanogaster depends on a CASK isoform containing CaMK-like and L27 domains AUTEN-67 (Autophagy Enhancer-67) Hampers the Progression of Neurodegenerative Symptoms in a Drosophila model of Huntington's Disease.A huntingtin peptide inhibits polyQ-huntingtin associated defects Human disease models in Drosophila melanogaster and the role of the fly in therapeutic drug discovery.Development of an ELISA assay for the quantification of soluble huntingtin in human blood cells.The role for alterations in neuronal activity in the pathogenesis of polyglutamine repeat disorders.Huntingtin aggregation kinetics and their pathological role in a Drosophila Huntington's disease model Drosophila models of proteinopathies: the little fly that could.DnaJ-1 and karyopherin α3 suppress degeneration in a new Drosophila model of Spinocerebellar Ataxia Type 6.Native mutant huntingtin in human brain: evidence for prevalence of full-length monomer Huntingtin proteolysis releases non-polyQ fragments that cause toxicity through dynamin 1 dysregulation.The small molecule AUTEN-99 (autophagy enhancer-99) prevents the progression of neurodegenerative symptoms.Novel BAC Mouse Model of Huntington's Disease with 225 CAG Repeats Exhibits an Early Widespread and Stable Degenerative Phenotype.Polyglutamine (polyQ) disorders: the chromatin connection.Early-onset sleep defects in Drosophila models of Huntington's disease reflect alterations of PKA/CREB signaling.Spinocerebellar ataxia type 6 knockin mice develop a progressive neuronal dysfunction with age-dependent accumulation of mutant CaV2.1 channels.Probing mechanisms that underlie human neurodegenerative diseases in Drosophila Dissociation of tau toxicity and phosphorylation: role of GSK-3beta, MARK and Cdk5 in a Drosophila model LRRK2 regulates retrograde synaptic compensation at the Drosophila neuromuscular junction.Symptomatic treatment of Huntington disease Aggregation formation in the polyglutamine diseases: protection at a cost?Ubiquitination regulates the neuroprotective function of the deubiquitinase ataxin-3 in vivo.Transglutaminase activation in neurodegenerative diseases.Mitochondrial structural and functional dynamics in Huntington's disease.Recent advances in using Drosophila to model neurodegenerative diseases.Drosophila and genome-wide association studies: a review and resource for the functional dissection of human complex traits.Drosophila melanogaster As a Model Organism to Study RNA Toxicity of Repeat Expansion-Associated Neurodegenerative and Neuromuscular Diseases Genetic mouse models of Huntington's disease: focus on electrophysiological mechanisms.The interrelationship between mitochondrial dysfunction and transcriptional dysregulation in Huntington disease.

P2860

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P2860

Suppression of neurodegeneration and increased neurotransmission caused by expanded full-length huntingtin accumulating in the cytoplasm

http://www.wikidata.org/entity/Q36514656

description

2008 nî lūn-bûn

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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2008年论文

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2008年论文

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name

Suppression of neurodegenerati ...... accumulating in the cytoplasm

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Suppression of neurodegenerati ...... accumulating in the cytoplasm

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type

label

Suppression of neurodegenerati ...... accumulating in the cytoplasm

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Suppression of neurodegenerati ...... accumulating in the cytoplasm

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prefLabel

Suppression of neurodegenerati ...... accumulating in the cytoplasm

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Suppression of neurodegenerati ...... accumulating in the cytoplasm

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J.NEURON.2007.11.025

P1433

P1476

Suppression of neurodegenerati ...... accumulating in the cytoplasm

@en

P2093

Cindy V Ly

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

Eliana Romero

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

Guang-Ho Cha

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

Juan Botas

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

Robert E Hughes

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 and huntingtin-associated protein 1 influence neuronal calcium signaling mediated by inositol-(1,4,5) triphosphate receptor type 1

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

SUMO modification of Huntingtin and Huntington's disease pathology

Cleavage of structural proteins during the assembly of the head of bacteriophage T4

A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes.

Targeted gene expression as a means of altering cell fates and generating dominant phenotypes

Synaptojanin is recruited by endophilin to promote synaptic vesicle uncoating

The hunt for huntingtin function: interaction partners tell many different stories

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27-40

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scholarly article

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10.1016/J.NEURON.2007.11.025

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1

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Patrik Verstreken

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5665301

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18184562

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2277511

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