Comparative analysis of genetic modifiers in Drosophila points to common and distinct mechanisms of pathogenesis among polyglutamine diseases. - Wikidata - awgldk - TriplyDB

Comparative analysis of genetic modifiers in Drosophila points to common and distinct mechanisms of pathogenesis among polyglutamine diseases.

Comparative analysis of genetic modifiers in Drosophila points to common and distinct mechanisms of pathogenesis among polyglutamine diseases.

http://www.wikidata.org/entity/Q45306884

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Improved activities of CREB binding protein, heterogeneous nuclear ribonucleoproteins and proteasome following downregulation of noncoding hsromega transcripts help suppress poly(Q) pathogenesis in fly models Animal models of polyglutamine diseases and therapeutic approaches Genetic modifiers of MeCP2 function in Drosophila.Huntingtin's function in axonal transport is conserved in Drosophila melanogaster Genetic background modulates behavioral impairments in R6/2 mice and suggests a role for dominant genetic modifiers in Huntington’s disease pathogenesis.Kismet/CHD7 regulates axon morphology, memory and locomotion in a Drosophila model of CHARGE syndrome.A potent and selective Sirtuin 1 inhibitor alleviates pathology in multiple animal and cell models of Huntington's disease.Polyglutamine toxicity in yeast induces metabolic alterations and mitochondrial defects Probing the metabolic aberrations underlying mutant huntingtin toxicity in yeast and assessing their degree of preservation in humans and mice.Small heat-shock proteins interact with a flanking domain to suppress polyglutamine aggregation.Neurodegenerative models in Drosophila: polyglutamine disorders, Parkinson disease, and amyotrophic lateral sclerosis.Identification of common genetic modifiers of neurodegenerative diseases from an integrative analysis of diverse genetic screens in model organisms FOX-2 dependent splicing of ataxin-2 transcript is affected by ataxin-1 overexpression Effete, an E2 ubiquitin-conjugating enzyme with multiple roles in Drosophila development and chromatin organization Categorizer: a tool to categorize genes into user-defined biological groups based on semantic similarity NeuroGeM, a knowledgebase of genetic modifiers in neurodegenerative diseases Drosophila models of proteinopathies: the little fly that could.Identification of novel genes that modify phenotypes induced by Alzheimer's beta-amyloid overexpression in Drosophila Polyglutamine neurodegeneration: protein misfolding revisited.Dissociation of tau toxicity and phosphorylation: role of GSK-3beta, MARK and Cdk5 in a Drosophila model Drosophila melanogaster as a model organism of brain diseases In vivo suppression of polyglutamine neurotoxicity by C-terminus of Hsp70-interacting protein (CHIP) supports an aggregation model of pathogenesis.Recent advances in using Drosophila to model neurodegenerative diseases.Neurodegenerative diseases: Lessons from genome-wide screens in small model organisms.Chaperones in Polyglutamine Aggregation: Beyond the Q-Stretch.Genetic modifiers of neurological disease Modifiers and mechanisms of multi-system polyglutamine neurodegenerative disorders: lessons from fly models.Repeat expansion diseases: when a good RNA turns bad.Cross-functional E3 ligases Parkin and C-terminus Hsp70-interacting protein in neurodegenerative disorders.Experimental models for identifying modifiers of polyglutamine-induced aggregation and neurodegeneration.Importance of gene dosage in controlling dendritic arbor formation during development.Studying polyglutamine diseases in Drosophila.PH domain leucine-rich repeat protein phosphatase 1 contributes to maintain the activation of the PI3K/Akt pro-survival pathway in Huntington's disease striatum.Exploring prion protein biology in flies: genetics and beyond.Lazarillo-related Lipocalins confer long-term protection against type I Spinocerebellar Ataxia degeneration contributing to optimize selective autophagy.Inhibition of PIP4Kγ ameliorates the pathological effects of mutant huntingtin protein.

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Comparative analysis of genetic modifiers in Drosophila points to common and distinct mechanisms of pathogenesis among polyglutamine diseases.

http://www.wikidata.org/entity/Q45306884

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2007 nî lūn-bûn

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Comparative analysis of geneti ...... among polyglutamine diseases.

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Comparative analysis of geneti ...... among polyglutamine diseases.

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Comparative analysis of geneti ...... among polyglutamine diseases.

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Comparative analysis of geneti ...... among polyglutamine diseases.

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Comparative analysis of geneti ...... among polyglutamine diseases.

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Comparative analysis of geneti ...... among polyglutamine diseases.

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Human Molecular Genetics

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Comparative analysis of geneti ...... among polyglutamine diseases.

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Alma M Pérez

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Diego Rincón-Limas

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Ismael Al-Ramahi

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Joana Branco

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Juan Botas

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Lubna Ukani

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Pedro Fernandez-Funez

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P2860

The spinocerebellar ataxia type 1 protein, ataxin-1, has RNA-binding activity that is inversely affected by the length of its polyglutamine tract

CHIP protects from the neurotoxicity of expanded and wild-type ataxin-1 and promotes their ubiquitination and degradation

14-3-3 protein interacts with Huntingtin-associated protein 1 and regulates its trafficking

Huntingtin and the molecular pathogenesis of Huntington's disease. Fourth in molecular medicine review series

The poly(C)-binding proteins: a multiplicity of functions and a search for mechanisms.

Homophila: human disease gene cognates in Drosophila

Phosphorylation of arfaptin 2 at Ser260 by Akt Inhibits PolyQ-huntingtin-induced toxicity by rescuing proteasome impairment

Association of missense and 5'-splice-site mutations in tau with the inherited dementia FTDP-17

Normal huntingtin function: an alternative approach to Huntington's disease

A neurotoxic peripherin splice variant in a mouse model of ALS

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376-390

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10.1093/HMG/DDM315

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3

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17

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