Mislocated FUS is sufficient for gain-of-toxic-function amyotrophic lateral sclerosis phenotypes in mice. - Wikidata - wikimedia - TriplyDB

Mislocated FUS is sufficient for gain-of-toxic-function amyotrophic lateral sclerosis phenotypes in mice.

Mislocated FUS is sufficient for gain-of-toxic-function amyotrophic lateral sclerosis phenotypes in mice.

http://www.wikidata.org/entity/Q48645659

about

Motor neuron intrinsic and extrinsic mechanisms contribute to the pathogenesis of FUS-associated amyotrophic lateral sclerosis.ALS-linked FUS exerts a gain of toxic function involving aberrant p38 MAPK activation.Expanding Axonal Transcriptome Brings New Functions for Axonally Synthesized Proteins in Health and Disease.Dendritic Homeostasis Disruption in a Novel Frontotemporal Dementia Mouse Model Expressing Cytoplasmic Fused in Sarcoma.De novo design of RNA-binding proteins with a prion-like domain related to ALS/FTD proteinopathies.RNA binding proteins and the pathological cascade in ALS/FTD neurodegeneration.To the end of the line: Axonal mRNA transport and local translation in health and neurodegenerative disease.Humanized mutant FUS drives progressive motor neuron degeneration without aggregation in 'FUSDelta14' knockin mice.Causative Genes in Amyotrophic Lateral Sclerosis and Protein Degradation Pathways: a Link to Neurodegeneration.Synaptic Paths to Neurodegeneration: The Emerging Role of TDP-43 and FUS in Synaptic Functions.Control of CNS functions by RNA-binding proteins in neurological diseases genetically interacts with the ALS-associated orthologue and mediates its toxicity

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P2860

Mislocated FUS is sufficient for gain-of-toxic-function amyotrophic lateral sclerosis phenotypes in mice.

http://www.wikidata.org/entity/Q48645659

description

2016 nî lūn-bûn

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2016年の論文

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2016年学术文章

@wuu

2016年学术文章

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2016年学术文章

@zh-cn

2016年学术文章

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2016年学术文章

@zh-my

2016年学术文章

@zh-sg

2016年學術文章

@yue

2016年學術文章

@zh-hant

name

Mislocated FUS is sufficient f ...... sclerosis phenotypes in mice.

@en

Mislocated FUS is sufficient f ...... sclerosis phenotypes in mice.

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type

label

Mislocated FUS is sufficient f ...... sclerosis phenotypes in mice.

@en

Mislocated FUS is sufficient f ...... sclerosis phenotypes in mice.

@nl

prefLabel

Mislocated FUS is sufficient f ...... sclerosis phenotypes in mice.

@en

Mislocated FUS is sufficient f ...... sclerosis phenotypes in mice.

@nl

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Mislocated FUS is sufficient f ...... sclerosis phenotypes in mice.

@en

P2093

Gen Shiihashi

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

Norihiro Suzuki

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

Taeko Ebine

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

Takuya Yagi

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

Yoshihiro Nihei

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

P2860

Abundant FUS-immunoreactive pathology in neuronal intermediate filament inclusion disease

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

Conjoint pathologic cascades mediated by ALS/FTLD-U linked RNA-binding proteins TDP-43 and FUS

A new subtype of frontotemporal lobar degeneration with FUS pathology

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

Mutations in the FUS/TLS gene on chromosome 16 cause familial amyotrophic lateral sclerosis

Mutations in FUS, an RNA processing protein, cause familial amyotrophic lateral sclerosis type 6

Mutations in the tail domain of DYNC1H1 cause dominant spinal muscular atrophy.

TDP-43 mutations in familial and sporadic amyotrophic lateral sclerosis

Microglia-specific localisation of a novel calcium binding protein, Iba1

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2380-2394

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10.1093/BRAIN/AWW161

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Pt 9

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139

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amyotrophic lateral sclerosis