Genome-wide screen for modifiers of ataxin-3 neurodegeneration in Drosophila - sprookjes - yvandenbroek - TriplyDB

Genome-wide screen for modifiers of ataxin-3 neurodegeneration in Drosophila

Genome-wide screen for modifiers of ataxin-3 neurodegeneration in Drosophila

http://www.wikidata.org/entity/Q27314808

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Identification of human proteins that modify misfolding and proteotoxicity of pathogenic ataxin-1 SCAMP5 links endoplasmic reticulum stress to the accumulation of expanded polyglutamine protein aggregates via endocytosis inhibition Animal models of polyglutamine diseases and therapeutic approaches Model systems of protein-misfolding diseases reveal chaperone modifiers of proteotoxicity Autophagy in polyglutamine disease: Imposing order on disorder or contributing to the chaos?Destabilizing protein polymorphisms in the genetic background direct phenotypic expression of mutant SOD1 toxicity A genetic screening strategy identifies novel regulators of the proteostasis network Modeling the complex pathology of Alzheimer's disease in Drosophila Drosophila as an In Vivo Model for Human Neurodegenerative Disease Therapeutic prospects for spinocerebellar ataxia type 2 and 3.Debra, a protein mediating lysosomal degradation, is required for long-term memory in Drosophila.Polyglutamine genes interact to modulate the severity and progression of neurodegeneration in Drosophila.Nucleocytoplasmic shuttling activity of ataxin-3.Modulation of heat shock transcription factor 1 as a therapeutic target for small molecule intervention in neurodegenerative disease Polyglutamine-rich suppressors of huntingtin toxicity act upstream of Hsp70 and Sti1 in spatial quality control of amyloid-like proteins.Uncoupling the Trade-Off between Somatic Proteostasis and Reproduction in Caenorhabditis elegans Models of Polyglutamine Diseases.Alzheimer's disease: insights from Drosophila melanogaster models.ASIP Outstanding Investigator Award Lecture. New approaches to the pathology and genetics of neurodegeneration Small heat-shock proteins interact with a flanking domain to suppress polyglutamine aggregation.Drosophila melanogaster in the study of human neurodegeneration.Neurodegenerative models in Drosophila: polyglutamine disorders, Parkinson disease, and amyotrophic lateral sclerosis.The mitochondrial chaperone protein TRAP1 mitigates α-Synuclein toxicity Identification of common genetic modifiers of neurodegenerative diseases from an integrative analysis of diverse genetic screens in model organisms The stress of protein misfolding: from single cells to multicellular organisms The aggregation and neurotoxicity of TDP-43 and its ALS-associated 25 kDa fragment are differentially affected by molecular chaperones in Drosophila.Heat shock factor 1 ameliorates proteotoxicity in cooperation with the transcription factor NFAT.Identification of the Drosophila ortholog of HSPB8: implication of HSPB8 loss of function in protein folding diseases.Genetic control of necrosis - another type of programmed cell death.Functional genomics in Drosophila models of human disease.Large-scale screen for modifiers of ataxin-3-derived polyglutamine-induced toxicity in Drosophila.Heat shock proteins and Drosophila aging.A cellular perspective on conformational disease: the role of genetic background and proteostasis networks.Rhomboid-7 and HtrA2/Omi act in a common pathway with the Parkinson's disease factors Pink1 and Parkin.Genome-wide screen for modifiers of Parkinson's disease genes in Drosophila.Regulation of autophagy by mTOR-dependent and mTOR-independent pathways: autophagy dysfunction in neurodegenerative diseases and therapeutic application of autophagy enhancers.NeuroGeM, a knowledgebase of genetic modifiers in neurodegenerative diseases Heat shock factor 2 is required for maintaining proteostasis against febrile-range thermal stress and polyglutamine aggregation.Pathogenic polyglutamine proteins cause dendrite defects associated with specific actin cytoskeletal alterations in Drosophila Functional genomic screen and network analysis reveal novel modifiers of tauopathy dissociated from tau phosphorylation.Genes and pathways affected by CAG-repeat RNA-based toxicity in Drosophila

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Genome-wide screen for modifiers of ataxin-3 neurodegeneration in Drosophila

http://www.wikidata.org/entity/Q27314808

description

2007 nî lūn-bûn

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2007 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

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2007 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2007年の論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年论文

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name

Genome-wide screen for modifiers of ataxin-3 neurodegeneration in Drosophila

@ast

Genome-wide screen for modifiers of ataxin-3 neurodegeneration in Drosophila

@en

Genome-wide screen for modifiers of ataxin-3 neurodegeneration in Drosophila

@nl

type

label

Genome-wide screen for modifiers of ataxin-3 neurodegeneration in Drosophila

@ast

Genome-wide screen for modifiers of ataxin-3 neurodegeneration in Drosophila

@en

Genome-wide screen for modifiers of ataxin-3 neurodegeneration in Drosophila

@nl

prefLabel

Genome-wide screen for modifiers of ataxin-3 neurodegeneration in Drosophila

@ast

Genome-wide screen for modifiers of ataxin-3 neurodegeneration in Drosophila

@en

Genome-wide screen for modifiers of ataxin-3 neurodegeneration in Drosophila

@nl

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Genome-wide screen for modifiers of ataxin-3 neurodegeneration in Drosophila

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An arginine/lysine-rich motif is crucial for VCP/p97-mediated modulation of ataxin-3 fibrillogenesis.

A protein-protein interaction network for human inherited ataxias and disorders of Purkinje cell degeneration

Cerebellar neurodegeneration in the absence of microRNAs

Ataxin-3 interactions with rad23 and valosin-containing protein and its associations with ubiquitin chains and the proteasome are consistent with a role in ubiquitin-mediated proteolysis

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

Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice

Loss of autophagy in the central nervous system causes neurodegeneration in mice

Inhibition of mTOR induces autophagy and reduces toxicity of polyglutamine expansions in fly and mouse models of Huntington disease

Caspase cleavage of gene products associated with triplet expansion disorders generates truncated fragments containing the polyglutamine tract

The roles of intracellular protein-degradation pathways in neurodegeneration

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