Fus gene mutations in familial and sporadic amyotrophic lateral sclerosis. - Wikidata - wikimedia - TriplyDB

Fus gene mutations in familial and sporadic amyotrophic lateral sclerosis.

Fus gene mutations in familial and sporadic amyotrophic lateral sclerosis.

http://www.wikidata.org/entity/Q34265540

about

ALS-associated fused in sarcoma (FUS) mutations disrupt Transportin-mediated nuclear import Sumoylation of critical proteins in amyotrophic lateral sclerosis: emerging pathways of pathogenesis FUS and TARDBP but not SOD1 interact in genetic models of amyotrophic lateral sclerosis Pathogenesis of FUS-associated ALS and FTD: insights from rodent models Oxr1 improves pathogenic cellular features of ALS-associated FUS and TDP-43 mutations A yeast model of FUS/TLS-dependent cytotoxicity.Distinct pathological subtypes of FTLD-FUS.De novo truncating FUS gene mutation as a cause of sporadic amyotrophic lateral sclerosis.FET proteins TAF15 and EWS are selective markers that distinguish FTLD with FUS pathology from amyotrophic lateral sclerosis with FUS mutations.The tip of the iceberg: RNA-binding proteins with prion-like domains in neurodegenerative disease.Activity-dependent FUS dysregulation disrupts synaptic homeostasis Aberrant RNA homeostasis in amyotrophic lateral sclerosis: potential for new therapeutic targets?Amyotrophic lateral sclerosis: one or multiple causes?Pathological heterogeneity in amyotrophic lateral sclerosis with FUS mutations: two distinct patterns correlating with disease severity and mutation Arginine methylation next to the PY-NLS modulates Transportin binding and nuclear import of FUS.The molecular basis of the frontotemporal lobar degeneration-amyotrophic lateral sclerosis spectrum ALS-associated mutant FUS induces selective motor neuron degeneration through toxic gain of function.ALS mutant FUS disrupts nuclear localization and sequesters wild-type FUS within cytoplasmic stress granules RNA-binding proteins in neurodegenerative disease: TDP-43 and beyond.Novel types of frontotemporal lobar degeneration: beyond tau and TDP-43.Clinical and genetic heterogeneity of amyotrophic lateral sclerosis.TARDBP and FUS mutations associated with amyotrophic lateral sclerosis: summary and update.Oligonucleotide-Based Therapy for FTD/ALS Caused by the C9orf72 Repeat Expansion: A Perspective.The role of FUS gene variants in neurodegenerative diseases.Loss and gain of FUS function impair neuromuscular synaptic transmission in a genetic model of ALS.Nuclear trafficking in amyotrophic lateral sclerosis and frontotemporal lobar degeneration.An autopsy case of frontotemporal lobar degeneration with the appearance of fused in sarcoma inclusions (basophilic inclusion body disease) clinically presenting corticobasal syndrome.Extra-motor abnormalities in amyotrophic lateral sclerosis: another layer of heterogeneity.RNA-binding proteins with prion-like domains in health and disease.Genotype-phenotype relationships in familial amyotrophic lateral sclerosis with FUS/TLS mutations in Japan.Novel FUS mutations identified through molecular screening in a large cohort of familial and sporadic amyotrophic lateral sclerosis.ALS-FUS pathology revisited: singleton FUS mutations and an unusual case with both a FUS and TARDBP mutation Evidence for an oligogenic basis of amyotrophic lateral sclerosis.Transportin 1 accumulates specifically with FET proteins but no other transportin cargos in FTLD-FUS and is absent in FUS inclusions in ALS with FUS mutations.Identification of ter94, Drosophila VCP, as a strong modulator of motor neuron degeneration induced by knockdown of Caz, Drosophila FUS.Humanized mutant FUS drives progressive motor neuron degeneration without aggregation in 'FUSDelta14' knockin mice.Astrocytes expressing ALS-linked mutant FUS induce motor neuron death through release of tumor necrosis factor-alpha.Looking for differences in copy number between blood and brain in sporadic amyotrophic lateral sclerosis.Biology and Pathobiology of TDP-43 and Emergent Therapeutic Strategies.Fused in Sarcoma Neuropathology in Neurodegenerative Disease.

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P2860

Fus gene mutations in familial and sporadic amyotrophic lateral sclerosis.

http://www.wikidata.org/entity/Q34265540

description

2010 nî lūn-bûn

@nan

2010 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի օգոստոսին հրատարակված գիտական հոդված

@hy

2010年の論文

@ja

2010年論文

@yue

2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

@wuu

name

Fus gene mutations in familial and sporadic amyotrophic lateral sclerosis.

@ast

Fus gene mutations in familial and sporadic amyotrophic lateral sclerosis.

@en

Fus gene mutations in familial and sporadic amyotrophic lateral sclerosis.

@nl

type

label

Fus gene mutations in familial and sporadic amyotrophic lateral sclerosis.

@ast

Fus gene mutations in familial and sporadic amyotrophic lateral sclerosis.

@en

Fus gene mutations in familial and sporadic amyotrophic lateral sclerosis.

@nl

prefLabel

Fus gene mutations in familial and sporadic amyotrophic lateral sclerosis.

@ast

Fus gene mutations in familial and sporadic amyotrophic lateral sclerosis.

@en

Fus gene mutations in familial and sporadic amyotrophic lateral sclerosis.

@nl

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P1433

Muscle and Nerve

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Fus gene mutations in familial and sporadic amyotrophic lateral sclerosis.

@en

P2093

Andrew Eisen

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

Charles Krieger

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

Hannah Briemberg

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

Heather Stewart

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

Ian R A Mackenzie

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

Mariely Dejesus-Hernandez

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

Marife Fabros

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

Neil Cashman

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

Neill Graff-Radford

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

P2860

Oncoprotein TLS interacts with serine-arginine proteins involved in RNA splicing

Fusion of CHOP to a novel RNA-binding protein in human myxoid liposarcoma

TLS/FUS, a pro-oncogene involved in multiple chromosomal translocations, is a novel regulator of BCR/ABL-mediated leukemogenesis.

MUSCLE: multiple sequence alignment with high accuracy and high throughput

Abundant FUS-immunoreactive pathology in neuronal intermediate filament inclusion disease

A new subtype of frontotemporal lobar degeneration with FUS pathology

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

Human POMp75 is identified as the pro-oncoprotein TLS/FUS: both POMp75 and POMp100 DNA homologous pairing activities are associated to cell proliferation

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

P304

170-176

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scholarly article

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10.1002/MUS.21665

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2

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42

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Rosa Rademakers

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2010-08-01T00:00:00Z

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44670185

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20544928

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P921

amyotrophic lateral sclerosis

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2969843

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