Knockdown of the Drosophila fused in sarcoma (FUS) homologue causes deficient locomotive behavior and shortening of motoneuron terminal branches.
about
Sumoylation of critical proteins in amyotrophic lateral sclerosis: emerging pathways of pathogenesisA loss of FUS/TLS function leads to impaired cellular proliferationThe ALS gene FUS regulates synaptic transmission at the Drosophila neuromuscular junction.Multistep process of FUS aggregation in the cell cytoplasm involves RNA-dependent and RNA-independent mechanisms.Characterization of FUS mutations in amyotrophic lateral sclerosis using RNA-Seq.ALS-associated FUS mutations result in compromised FUS alternative splicing and autoregulation.A fruitful endeavor: modeling ALS in the fruit flyMechanisms of disease in frontotemporal lobar degeneration: gain of function versus loss of function effectsHighly efficient targeted mutagenesis in mice using TALENsDefects in synapse structure and function precede motor neuron degeneration in Drosophila models of FUS-related ALS.Protein aggregation in amyotrophic lateral sclerosis.Nuclear transcription factor Y and its roles in cellular processes related to human disease.The role of FUS gene variants in neurodegenerative diseases.Worming forward: amyotrophic lateral sclerosis toxicity mechanisms and genetic interactions in Caenorhabditis elegans.Drosophila as a model to study the role of glia in neurodegeneration.Simple animal models for amyotrophic lateral sclerosis drug discovery.FET proteins regulate lifespan and neuronal integrity.RNA Granules and Diseases: A Case Study of Stress Granules in ALS and FTLDFUS toxicity is rescued by the modulation of lncRNA hsrω expression in Drosophila melanogaster.Identification of ter94, Drosophila VCP, as a strong modulator of motor neuron degeneration induced by knockdown of Caz, Drosophila FUS.Neuron-specific knockdown of the Drosophila fat induces reduction of life span, deficient locomotive ability, shortening of motoneuron terminal branches and defects in axonal targeting.Overexpression of ter94, Drosophila VCP, improves motor neuron degeneration induced by knockdown of TBPH, Drosophila TDP-43.Importance of Functional Loss of FUS in FTLD/ALS.as a Model for Assessing the Function of RNA-Binding Proteins during Neurogenesis and Neurological Disease
P2860
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P2860
Knockdown of the Drosophila fused in sarcoma (FUS) homologue causes deficient locomotive behavior and shortening of motoneuron terminal branches.
description
2012 nî lūn-bûn
@nan
2012 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
2012 թվականի հունիսին հրատարակված գիտական հոդված
@hy
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
name
Knockdown of the Drosophila fu ...... motoneuron terminal branches.
@ast
Knockdown of the Drosophila fu ...... motoneuron terminal branches.
@en
Knockdown of the Drosophila fused in sarcoma
@nl
type
label
Knockdown of the Drosophila fu ...... motoneuron terminal branches.
@ast
Knockdown of the Drosophila fu ...... motoneuron terminal branches.
@en
Knockdown of the Drosophila fused in sarcoma
@nl
prefLabel
Knockdown of the Drosophila fu ...... motoneuron terminal branches.
@ast
Knockdown of the Drosophila fu ...... motoneuron terminal branches.
@en
Knockdown of the Drosophila fused in sarcoma
@nl
P2093
P2860
P1433
P1476
Knockdown of the Drosophila fu ...... f motoneuron terminal branches
@en
P2093
Hiroshi Sasayama
Mai Shimamura
Masamitsu Yamaguchi
Masanori Nakagawa
Nobuhiro Fujikake
Takahiko Tokuda
Tomokatsu Yoshida
Yoshitaka Nagai
Yumiko Azuma
P2860
P304
P356
10.1371/JOURNAL.PONE.0039483
P407
P577
2012-06-19T00:00:00Z