Aggregation formation in the polyglutamine diseases: protection at a cost? - Wikidata - awgldk - TriplyDB

Aggregation formation in the polyglutamine diseases: protection at a cost?

Aggregation formation in the polyglutamine diseases: protection at a cost?

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The sodium leak channel, NALCN, in health and disease Beyond the glutamine expansion: influence of posttranslational modifications of ataxin-1 in the pathogenesis of spinocerebellar ataxia type 1 Motor Dysfunctions and Neuropathology in Mouse Models of Spinocerebellar Ataxia Type 2: A Comprehensive Review Poly(Q) Expansions in ATXN7 Affect Solubility but Not Activity of the SAGA Deubiquitinating Module The aggregation and inheritance of damaged proteins determines cell fate during mitosis.A knockin mouse model of spinocerebellar ataxia type 3 exhibits prominent aggregate pathology and aberrant splicing of the disease gene transcript.Polyglutamine- and temperature-dependent conformational rigidity in mutant huntingtin revealed by immunoassays and circular dichroism spectroscopy Nemo-like kinase is a novel regulator of spinal and bulbar muscular atrophy.Enhanced molecular mobility of ordinarily structured regions drives polyglutamine disease C9ORF72 poly(GA) aggregates sequester and impair HR23 and nucleocytoplasmic transport proteins.Potential therapeutic targets in polyglutamine-mediated diseases.Nanoparticulate strategies for the treatment of polyglutamine diseases by halting the protein aggregation process.Mutation-dependent aggregation and toxicity in a Drosophila model for UBQLN2-associated ALS.Autophagy mediates SUMO-induced degradation of a polyglutamine protein ataxin-3

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Aggregation formation in the polyglutamine diseases: protection at a cost?

http://www.wikidata.org/entity/Q37238530

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article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 19 June 2013

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Aggregation formation in the polyglutamine diseases: protection at a cost?

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Aggregation formation in the polyglutamine diseases: protection at a cost?

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Aggregation formation in the polyglutamine diseases: protection at a cost?

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Aggregation formation in the polyglutamine diseases: protection at a cost?

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Aggregation formation in the polyglutamine diseases: protection at a cost?

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Aggregation formation in the polyglutamine diseases: protection at a cost?

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Molecules and Cells

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Aggregation formation in the polyglutamine diseases: protection at a cost?

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Janghoo Lim

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Tiffany W Todd

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

Ataxin-1 with an expanded glutamine tract alters nuclear matrix-associated structures

Amyloids: friend or foe?

Huntingtin aggregation and toxicity in Huntington's disease

Formation of neuronal intranuclear inclusions underlies the neurological dysfunction in mice transgenic for the HD mutation

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

Co-induction of the heat shock response ameliorates disease progression in a mouse model of human spinal and bulbar muscular atrophy: implications for therapy

Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death

Trinucleotide Repeat Disorders

Inherent toxicity of aggregates implies a common mechanism for protein misfolding diseases

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185-194

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scholarly article

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10.1007/S10059-013-0167-X

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2013-06-19T00:00:00Z

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