A Drosophila model of FUS-related neurodegeneration reveals genetic interaction between FUS and TDP-43. - Wikidata - thesis-toulmin - TriplyDB

A Drosophila model of FUS-related neurodegeneration reveals genetic interaction between FUS and TDP-43.

A Drosophila model of FUS-related neurodegeneration reveals genetic interaction between FUS and TDP-43.

http://www.wikidata.org/entity/Q34882752

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Evaluating the role of the FUS/TLS-related gene EWSR1 in amyotrophic lateral sclerosis From animal models to human disease: a genetic approach for personalized medicine in ALS Mechanisms of FUS mutations in familial amyotrophic lateral sclerosis The function of RNA-binding proteins at the synapse: implications for neurodegeneration Mutant TDP-43 and FUS cause age-dependent paralysis and neurodegeneration in C. elegans Regulation of protein quality control by UBE4B and LSD1 through p53-mediated transcription 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 Drosophila as an In Vivo Model for Human Neurodegenerative Disease FUS Interacts with HSP60 to Promote Mitochondrial Damage Protein arginine methyltransferase 6 enhances polyglutamine-expanded androgen receptor function and toxicity in spinal and bulbar muscular atrophy.Methods to assay Drosophila behavior.Overexpression of human wild-type FUS causes progressive motor neuron degeneration in an age- and dose-dependent fashion.Modelling amyotrophic lateral sclerosis: progress and possibilities The ALS gene FUS regulates synaptic transmission at the Drosophila neuromuscular junction.Using membrane-targeted green fluorescent protein to monitor neurotoxic protein-dependent degeneration of Drosophila eyes Multistep process of FUS aggregation in the cell cytoplasm involves RNA-dependent and RNA-independent mechanisms.Knockdown of the Drosophila fused in sarcoma (FUS) homologue causes deficient locomotive behavior and shortening of motoneuron terminal branches.Mechanisms, models and biomarkers in amyotrophic lateral sclerosis Activity-dependent FUS dysregulation disrupts synaptic homeostasis Pur-alpha regulates cytoplasmic stress granule dynamics and ameliorates FUS toxicity.Motor neurons and glia exhibit specific individualized responses to TDP-43 expression in a Drosophila model of amyotrophic lateral sclerosis.Characterization of FUS mutations in amyotrophic lateral sclerosis using RNA-Seq.Protein arginine methyltransferase 1 and 8 interact with FUS to modify its sub-cellular distribution and toxicity in vitro and in vivo.Opposing roles of p38 and JNK in a Drosophila model of TDP-43 proteinopathy reveal oxidative stress and innate immunity as pathogenic components of neurodegeneration.What we can learn from animal models about cerebral multi-morbidity.PPAR gamma activation is neuroprotective in a Drosophila model of ALS based on TDP-43.A fruitful endeavor: modeling ALS in the fruit fly Model systems of motor neuron diseases as a platform for studying pathogenic mechanisms and searching for therapeutic agents.Advances in imaging ultrastructure yield new insights into presynaptic biology A yeast functional screen predicts new candidate ALS disease genes Gains or losses: molecular mechanisms of TDP43-mediated neurodegeneration.DnaJ-1 and karyopherin α3 suppress degeneration in a new Drosophila model of Spinocerebellar Ataxia Type 6.Motor neuron apoptosis and neuromuscular junction perturbation are prominent features in a Drosophila model of Fus-mediated ALS Antisense proline-arginine RAN dipeptides linked to C9ORF72-ALS/FTD form toxic nuclear aggregates that initiate in vitro and in vivo neuronal death.Retrotransposon activation contributes to neurodegeneration in a Drosophila TDP-43 model of ALS Entorhinal cortical neurons are the primary targets of FUS mislocalization and ubiquitin aggregation in FUS transgenic rats.TDP-43 and FUS en route from the nucleus to the cytoplasm.Lack of miRNA Misregulation at Early Pathological Stages in Drosophila Neurodegenerative Disease Models.Expression of Fused in sarcoma mutations in mice recapitulates the neuropathology of FUS proteinopathies and provides insight into disease pathogenesis.

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A Drosophila model of FUS-related neurodegeneration reveals genetic interaction between FUS and TDP-43.

http://www.wikidata.org/entity/Q34882752

description

2011 nî lūn-bûn

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2011 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2011 թվականի ապրիլին հրատարակված գիտական հոդված

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2011年の論文

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年學術文章

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A Drosophila model of FUS-rela ...... action between FUS and TDP-43.

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A Drosophila model of FUS-rela ...... action between FUS and TDP-43.

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A Drosophila model of FUS-rela ...... action between FUS and TDP-43.

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type

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A Drosophila model of FUS-rela ...... action between FUS and TDP-43.

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A Drosophila model of FUS-rela ...... action between FUS and TDP-43.

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A Drosophila model of FUS-rela ...... action between FUS and TDP-43.

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A Drosophila model of FUS-rela ...... action between FUS and TDP-43.

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A Drosophila model of FUS-rela ...... action between FUS and TDP-43.

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A Drosophila model of FUS-rela ...... action between FUS and TDP-43.

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Human Molecular Genetics

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A Drosophila model of FUS-rela ...... raction between FUS and TDP-43

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Astha Maltare

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Hanna King

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Ji Han Kim

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Nicholas A Lanson

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Rebecca Smith

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Udai Bhan Pandey

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P2860

Modeling spinal muscular atrophy in Drosophila

The Microprocessor complex mediates the genesis of microRNAs

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

dAtaxin-2 mediates expanded Ataxin-1-induced neurodegeneration in a Drosophila model of SCA1

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

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

TLS (FUS) binds RNA in vivo and engages in nucleo-cytoplasmic shuttling

TDP-43 mutations in familial and sporadic amyotrophic lateral sclerosis

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10.1093/HMG/DDR150

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13

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20

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Thomas E. Lloyd

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