Progressive disruption of cellular protein folding in models of polyglutamine diseases.
about
Prion switching in response to environmental stressSystematic in vivo analysis of the intrinsic determinants of amyloid Beta pathogenicityChaperone-like activity of high-mobility group box 1 protein and its role in reducing the formation of polyglutamine aggregatesThe 8 and 5 kDa fragments of plasma gelsolin form amyloid fibrils by a nucleated polymerization mechanism, while the 68 kDa fragment is not amyloidogenicMutant LRRK2 toxicity in neurons depends on LRRK2 levels and synuclein but not kinase activity or inclusion bodiesSUT-2 potentiates tau-induced neurotoxicity in Caenorhabditis elegansSecretion of amyloidogenic gelsolin progressively compromises protein homeostasis leading to the intracellular aggregation of proteinsAging as an event of proteostasis collapseCollapse of proteostasis represents an early molecular event in Caenorhabditis elegans agingMisfolded proteins partition between two distinct quality control compartmentsAnimal models of polyglutamine diseases and therapeutic approachesProtein homeostasis and aging: taking care of proteins from the cradle to the graveModel systems of protein-misfolding diseases reveal chaperone modifiers of proteotoxicityMolecular chaperones: guardians of the proteome in normal and disease statesRegulation of protein homeostasis in neurodegenerative diseases: the role of coding and non-coding genesFOXO transcription factors: key regulators of cellular quality controlProtein homeostasis as a therapeutic target for diseases of protein conformationChemical and biological approaches for adapting proteostasis to ameliorate protein misfolding and aggregation diseases: progress and prognosisRegulation of cellular protein quality control networks in a multicellular organismHuntington's disease: underlying molecular mechanisms and emerging conceptsInvestigating the spreading and toxicity of prion-like proteins using the metazoan model organism C. elegansDestabilizing protein polymorphisms in the genetic background direct phenotypic expression of mutant SOD1 toxicityModulation of the maladaptive stress response to manage diseases of protein foldingGenome-wide screen for modifiers of ataxin-3 neurodegeneration in DrosophilaHsp90 selectively modulates phenotype in vertebrate developmentNeuronal reprograming of protein homeostasis by calcium-dependent regulation of the heat shock responseIndividual and collective contributions of chaperoning and degradation to protein homeostasis in E. coli.Widespread protein aggregation as an inherent part of aging in C. elegansSpreading of a prion domain from cell-to-cell by vesicular transport in Caenorhabditis elegansFluorodeoxyuridine improves Caenorhabditis elegans proteostasis independent of reproduction onsetNovel polyglutamine model uncouples proteotoxicity from agingA genetic screening strategy identifies novel regulators of the proteostasis networkToward Optimization of the Second Aryl Substructure Common to Transthyretin Amyloidogenesis Inhibitors Using Biochemical and Structural Studies †Conformational Conversion during Amyloid Formation at Atomic ResolutionSmall molecule probes to quantify the functional fraction of a specific protein in a cell with minimal folding equilibrium shiftsThe struggle by Caenorhabditis elegans to maintain proteostasis during aging and diseaseA chaperome subnetwork safeguards proteostasis in aging and neurodegenerative diseaseIntegrating the stress response: lessons for neurodegenerative diseases from C. elegansAggregation of human S100A8 and S100A9 amyloidogenic proteins perturbs proteostasis in a yeast modelIn vivo substrates of the lens molecular chaperones αA-crystallin and αB-crystallin
P2860
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P2860
Progressive disruption of cellular protein folding in models of polyglutamine diseases.
description
2006 nî lūn-bûn
@nan
2006 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2006 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
name
Progressive disruption of cellular protein folding in models of polyglutamine diseases.
@ast
Progressive disruption of cellular protein folding in models of polyglutamine diseases.
@en
Progressive disruption of cellular protein folding in models of polyglutamine diseases.
@nl
type
label
Progressive disruption of cellular protein folding in models of polyglutamine diseases.
@ast
Progressive disruption of cellular protein folding in models of polyglutamine diseases.
@en
Progressive disruption of cellular protein folding in models of polyglutamine diseases.
@nl
prefLabel
Progressive disruption of cellular protein folding in models of polyglutamine diseases.
@ast
Progressive disruption of cellular protein folding in models of polyglutamine diseases.
@en
Progressive disruption of cellular protein folding in models of polyglutamine diseases.
@nl
P2093
P356
P1433
P1476
Progressive disruption of cellular protein folding in models of polyglutamine diseases
@en
P2093
Heather R Brignull
Richard I Morimoto
P304
P356
10.1126/SCIENCE.1124514
P407
P577
2006-02-09T00:00:00Z