Pivotal role of oligomerization in expanded polyglutamine neurodegenerative disorders.
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Simple sequence repeats provide a substrate for phenotypic variation in the Neurospora crassa circadian clockIdentification of potential therapeutic drugs for huntington's disease using Caenorhabditis elegansThe RIP1/RIP3 necrosome forms a functional amyloid signaling complex required for programmed necrosisSCAMP5 links endoplasmic reticulum stress to the accumulation of expanded polyglutamine protein aggregates via endocytosis inhibitionPML clastosomes prevent nuclear accumulation of mutant ataxin-7 and other polyglutamine proteinsAsialoerythropoietin is not effective in the R6/2 line of Huntington's disease miceMolecular origin of polyglutamine aggregation in neurodegenerative diseases.Overview of Alzheimer's Disease and Some Therapeutic Approaches Targeting Aβ by Using Several Synthetic and Herbal CompoundsThe many faces of autophagy dysfunction in Huntington's disease: from mechanism to therapyMouse models of polyglutamine diseases in therapeutic approaches: review and data table. Part II.Therapeutic Approaches for Inhibition of Protein Aggregation in Huntington's DiseaseComparative study of naturally occurring huntingtin fragments in Drosophila points to exon 1 as the most pathogenic species in Huntington's diseaseThe amyloid-Congo red interface at atomic resolutionBeta conformation of polyglutamine track revealed by a crystal structure of Huntingtin N-terminal region with insertion of three histidine residuesHuntingtin and its role in neuronal degenerationRegulation of proteasome activity in health and diseaseNetwork-based identification of biomarkers coexpressed with multiple pathwaysTissue transglutaminase contributes to disease progression in the R6/2 Huntington's disease mouse model via aggregate-independent mechanismsRNA-binding protein is involved in aggregation of light neurofilament protein and is implicated in the pathogenesis of motor neuron degenerationTemporal separation of aggregation and ubiquitination during early inclusion formation in transgenic mice carrying the Huntington's disease mutationAmyloid-like fibril formation by polyQ proteins: a critical balance between the polyQ length and the constraints imposed by the host proteinTherapeutic prospects for spinocerebellar ataxia type 2 and 3.Mitochondrial quality, dynamics and functional capacity in Parkinson's disease cybrid cell lines selected for Lewy body expression.Improvement of neuropathology and transcriptional deficits in CAG 140 knock-in mice supports a beneficial effect of dietary curcumin in Huntington's disease.Intrabody gene therapy ameliorates motor, cognitive, and neuropathological symptoms in multiple mouse models of Huntington's disease.Formation and toxicity of soluble polyglutamine oligomers in living cells.Anthraquinones inhibit tau aggregation and dissolve Alzheimer's paired helical filaments in vitro and in cells.Short G-rich oligonucleotides as a potential therapeutic for Huntington's DiseasePolyglutamine expansion mutation yields a pathological epitope linked to nucleation of protein aggregate: determinant of Huntington's disease onset.Small molecule regulators of autophagy identified by an image-based high-throughput screen.The ubiquitin proteasome system in Huntington's disease and the spinocerebellar ataxiasMolecular pathogenesis and cellular pathology of spinocerebellar ataxia type 7 neurodegenerationStable polyglutamine dimers can contain β-hairpins with interdigitated side chains-but not α-helices, β-nanotubes, β-pseudohelices, or steric zippers.A potent small molecule inhibits polyglutamine aggregation in Huntington's disease neurons and suppresses neurodegeneration in vivo.Therapeutic Strategies in Huntington's DiseaseA two-step path to inclusion formation of huntingtin peptides revealed by number and brightness analysis.Suppression of Huntington's disease pathology in Drosophila by human single-chain Fv antibodies.RNA interference improves motor and neuropathological abnormalities in a Huntington's disease mouse model.Modifiers of mutant huntingtin aggregation: functional conservation of C. elegans-modifiers of polyglutamine aggregation.Neuroprotective potential of CB1 receptor agonists in an in vitro model of Huntington's disease.
P2860
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P2860
Pivotal role of oligomerization in expanded polyglutamine neurodegenerative disorders.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年学术文章
@wuu
2003年学术文章
@zh
2003年学术文章
@zh-cn
2003年学术文章
@zh-hans
2003年学术文章
@zh-my
2003年学术文章
@zh-sg
2003年學術文章
@yue
2003年學術文章
@zh-hant
name
Pivotal role of oligomerization in expanded polyglutamine neurodegenerative disorders.
@en
Pivotal role of oligomerization in expanded polyglutamine neurodegenerative disorders.
@nl
type
label
Pivotal role of oligomerization in expanded polyglutamine neurodegenerative disorders.
@en
Pivotal role of oligomerization in expanded polyglutamine neurodegenerative disorders.
@nl
prefLabel
Pivotal role of oligomerization in expanded polyglutamine neurodegenerative disorders.
@en
Pivotal role of oligomerization in expanded polyglutamine neurodegenerative disorders.
@nl
P356
P1433
P1476
Pivotal role of oligomerization in expanded polyglutamine neurodegenerative disorders
@en
P2093
Christian Mahlke
Junying Yuan
P2888
P304
P356
10.1038/NATURE01301
P407
P577
2003-01-01T00:00:00Z
P5875
P6179
1017653700