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

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

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

http://www.wikidata.org/entity/Q27314605

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Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS Comparison of an expanded ataxia interactome with patient medical records reveals a relationship between macular degeneration and ataxia Animal models of polyglutamine diseases and therapeutic approaches Motor Dysfunctions and Neuropathology in Mouse Models of Spinocerebellar Ataxia Type 2: A Comprehensive Review A genome-scale RNA-interference screen identifies RRAS signaling as a pathologic feature of Huntington's disease Bacteria, yeast, worms, and flies: exploiting simple model organisms to investigate human mitochondrial diseases Ataxin-2 modulates the levels of Grb2 and SRC but not ras signaling.Polyglutamine genes interact to modulate the severity and progression of neurodegeneration in Drosophila.Guide to understanding Drosophila models of neurodegenerative diseases.Dissociated fear and spatial learning in mice with deficiency of ataxin-2 RAS-MAPK-MSK1 pathway modulates ataxin 1 protein levels and toxicity in SCA1 Conserved genes act as modifiers of invertebrate SMN loss of function defects Ataxin-2: From RNA Control to Human Health and Disease Drosophila melanogaster in the study of human neurodegeneration.Neurodegenerative models in Drosophila: polyglutamine disorders, Parkinson disease, and amyotrophic lateral sclerosis.Using membrane-targeted green fluorescent protein to monitor neurotoxic protein-dependent degeneration of Drosophila eyes FOX-2 dependent splicing of ataxin-2 transcript is affected by ataxin-1 overexpression ATXN2-CAG42 sequesters PABPC1 into insolubility and induces FBXW8 in cerebellum of old ataxic knock-in mice.Ataxin-2 intermediate-length polyglutamine expansions in European ALS patients A Drosophila model of FUS-related neurodegeneration reveals genetic interaction between FUS and TDP-43.NeuroGeM, a knowledgebase of genetic modifiers in neurodegenerative diseases Epigenetics as an answer to Darwin's "special difficulty," Part 2: natural selection of metastable epialleles in honeybee castes.Protein interactome reveals converging molecular pathways among autism disorders.Protein interacting with C kinase (PICK1) is a suppressor of spinocerebellar ataxia 3-associated neurodegeneration in Drosophila.Drosophila models of proteinopathies: the little fly that could.A functional deficiency of TERA/VCP/p97 contributes to impaired DNA repair in multiple polyglutamine diseases Genetic circuitry of Survival motor neuron, the gene underlying spinal muscular atrophy Drosophila ataxin-2 gene encodes two differentially expressed isoforms and its function in larval fat body is crucial for development of peripheral tissues Dysregulation of mRNA Localization and Translation in Genetic Disease Recent advances in using Drosophila to model neurodegenerative diseases.FMRP and Ataxin-2 function together in long-term olfactory habituation and neuronal translational control.Ubx promotes corbicular development in Apis mellifera Neurodegenerative diseases: Lessons from genome-wide screens in small model organisms.Modifiers and mechanisms of multi-system polyglutamine neurodegenerative disorders: lessons from fly models.Local RNA translation at the synapse and in disease.Atxn2 Knockout and CAG42-Knock-in Cerebellum Shows Similarly Dysregulated Expression in Calcium Homeostasis Pathway.Concurrent CIC mutations, IDH mutations, and 1p/19q loss distinguish oligodendrogliomas from other cancers.Ataxin-2 (Atxn2)-Knock-Out Mice Show Branched Chain Amino Acids and Fatty Acids Pathway Alterations.Re-establishing ataxin-2 downregulates translation of mutant ataxin-3 and alleviates Machado-Joseph disease.Spinocerebellar Ataxia Type 2: Clinicogenetic Aspects, Mechanistic Insights, and Management Approaches.

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

http://www.wikidata.org/entity/Q27314605

description

2007 nî lūn-bûn

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2007 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

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2007 թվականի դեկտեմբերին հրատարակված գիտական հոդված

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Alma M Pérez

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Ismael Al-Ramahi

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Janghoo Lim

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Joana Branco

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Juan Botas

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Minghang Zhang

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Rie Sorensen

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Stefan M Pulst

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P2860

Huntingtin interacting proteins are genetic modifiers of neurodegeneration

Towards a proteome-scale map of the human protein–protein interaction network

Nuclear localization or inclusion body formation of ataxin-2 are not necessary for SCA2 pathogenesis in mouse or human

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

Ataxin-2 and its Drosophila homolog, ATX2, physically assemble with polyribosomes

Ataxin-2 interacts with the DEAD/H-box RNA helicase DDX6 and interferes with P-bodies and stress granules

Expansion of the polyQ repeat in ataxin-2 alters its Golgi localization, disrupts the Golgi complex and causes cell death

Ataxin 1, a SCA1 neurodegenerative disorder protein, is functionally linked to the silencing mediator of retinoid and thyroid hormone receptors

Cloning of the gene for spinocerebellar ataxia 2 reveals a locus with high sensitivity to expanded CAG/glutamine repeats

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

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