Entorhinal cortical neurons are the primary targets of FUS mislocalization and ubiquitin aggregation in FUS transgenic rats. - Test2 - elhamkhani - TriplyDB

Entorhinal cortical neurons are the primary targets of FUS mislocalization and ubiquitin aggregation in FUS transgenic rats.

Entorhinal cortical neurons are the primary targets of FUS mislocalization and ubiquitin aggregation in FUS transgenic rats.

http://www.wikidata.org/entity/Q36317708

about

Pathogenic mutation of UBQLN2 impairs its interaction with UBXD8 and disrupts endoplasmic reticulum-associated protein degradation Mechanisms of FUS mutations in familial amyotrophic lateral sclerosis Oxidative stress and mitochondrial damage: importance in non-SOD1 ALS Pathogenesis of FUS-associated ALS and FTD: insights from rodent models Expression of ALS-linked TDP-43 mutant in astrocytes causes non-cell-autonomous motor neuron death in rats Profiling the genes affected by pathogenic TDP-43 in astrocytes Aging differentially affects the loss of neuronal dendritic spine, neuroinflammation and memory impairment at rats after surgery.A single administration of human umbilical cord blood T cells produces long-lasting effects in the aging hippocampus A fruitful endeavor: modeling ALS in the fruit fly Evidence of Mitochondrial Dysfunction within the Complex Genetic Etiology of Schizophrenia.XBP1 depletion precedes ubiquitin aggregation and Golgi fragmentation in TDP-43 transgenic rats.Pathogenic mutation in VPS35 impairs its protection against MPP(+) cytotoxicity Pathogenic Ubqln2 gains toxic properties to induce neuron death.Reactive astrocytes secrete lcn2 to promote neuron death.Changes in the Expression of FUS/TLS in Spinal Cords of SOD1 G93A Transgenic Mice and Correlation with Motor-Neuron Degeneration.The role of FUS gene variants in neurodegenerative diseases.AMPK Signalling and Defective Energy Metabolism in Amyotrophic Lateral Sclerosis.Targeting mitochondrial metal dyshomeostasis for the treatment of neurodegeneration.Advances in the Development of Disease-Modifying Treatments for Amyotrophic Lateral Sclerosis.The role of endoplasmic reticulum stress in neurodegenerative disease.Golgi fragmentation precedes neuromuscular denervation and is associated with endosome abnormalities in SOD1-ALS mouse motor neurons.ALS/FTD-associated FUS activates GSK-3β to disrupt the VAPB-PTPIP51 interaction and ER-mitochondria associations.Mitochondrial quality control in amyotrophic lateral sclerosis: towards a common pathway?Increased Ubqln2 expression causes neuron death in transgenic rats Mitochondrial abnormalities and disruption of the neuromuscular junction precede the clinical phenotype and motor neuron loss in hFUSWT transgenic mice.Role and Therapeutic Potential of Astrocytes in Amyotrophic Lateral Sclerosis.Energy metabolism in ALS: an underappreciated opportunity?Synaptic Paths to Neurodegeneration: The Emerging Role of TDP-43 and FUS in Synaptic Functions.Amyotrophic Lateral Sclerosis associated FUS mutation shortens mitochondria and induces neurotoxicity Neurodegeneration-associated FUS is a novel regulator of circadian gene expression From Mouse Models to Human Disease: An Approach for Amyotrophic Lateral Sclerosis

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P2860

Entorhinal cortical neurons are the primary targets of FUS mislocalization and ubiquitin aggregation in FUS transgenic rats.

http://www.wikidata.org/entity/Q36317708

description

2012 nî lūn-bûn

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2012年の論文

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2012年学术文章

@wuu

2012年学术文章

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2012年学术文章

@zh-hans

2012年学术文章

@zh-my

2012年学术文章

@zh-sg

2012年學術文章

@yue

2012年學術文章

@zh

2012年學術文章

@zh-hant

name

Entorhinal cortical neurons ar ...... gation in FUS transgenic rats.

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Entorhinal cortical neurons ar ...... gation in FUS transgenic rats.

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type

label

Entorhinal cortical neurons ar ...... gation in FUS transgenic rats.

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Entorhinal cortical neurons ar ...... gation in FUS transgenic rats.

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prefLabel

Entorhinal cortical neurons ar ...... gation in FUS transgenic rats.

@ast

Entorhinal cortical neurons ar ...... gation in FUS transgenic rats.

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Human Molecular Genetics

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Entorhinal cortical neurons ar ...... gation in FUS transgenic rats.

@en

P2093

Bo Huang

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

Cao Huang

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

Fangfang Bi

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

Hongxia Zhou

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

Jianbin Tong

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

Qinxue Wu

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

Xu-Gang Xia

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

P2860

ALS-associated fused in sarcoma (FUS) mutations disrupt Transportin-mediated nuclear import

Induced ncRNAs allosterically modify RNA-binding proteins in cis to inhibit transcription

A new subtype of frontotemporal lobar degeneration with FUS pathology

Rosiglitazone increases dendritic spine density and rescues spine loss caused by apolipoprotein E4 in primary cortical neurons

Mutant TDP-43 and FUS cause age-dependent paralysis and neurodegeneration in C. elegans

FUS and TARDBP but not SOD1 interact in genetic models of amyotrophic lateral sclerosis

FUS transgenic rats develop the phenotypes of amyotrophic lateral sclerosis and frontotemporal lobar degeneration

Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis

Human 75-kDa DNA-pairing protein is identical to the pro-oncoprotein TLS/FUS and is able to promote D-loop formation

Identification of an RNA binding specificity for the potential splicing factor TLS

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4602-4614

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scholarly article

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10.1093/HMG/DDS299

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21

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21

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2012-07-23T00:00:00Z

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22833456

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3471393

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