Live-cell imaging reveals divergent intracellular dynamics of polyglutamine disease proteins and supports a sequestration model of pathogenesis.
about
Identification of human proteins that modify misfolding and proteotoxicity of pathogenic ataxin-1Quantitative fluorescence loss in photobleaching for analysis of protein transport and aggregation.Valosin-containing protein (VCP/p97) is an activator of wild-type ataxin-3The DNAJB6 and DNAJB8 protein chaperones prevent intracellular aggregation of polyglutamine peptidesNuclear transport, oxidative stress, and neurodegenerationCell biology of spinocerebellar ataxiaA series of N-terminal epitope tagged Hdh knock-in alleles expressing normal and mutant huntingtin: their application to understanding the effect of increasing the length of normal Huntingtin's polyglutamine stretch on CAG140 mouse model pathogenesiNuclear aggresomes form by fusion of PML-associated aggregates.Formation and toxicity of soluble polyglutamine oligomers in living cells.Conformational targeting of fibrillar polyglutamine proteins in live cells escalates aggregation and cytotoxicity.Nucleocytoplasmic shuttling activity of ataxin-3.Ataxin-3 promotes genome integrity by stabilizing Chk1.Splice isoforms of the polyglutamine disease protein ataxin-3 exhibit similar enzymatic yet different aggregation properties.Systemic delivery of P42 peptide: a new weapon to fight Huntington's disease.Sequestration of cellular interacting partners by protein aggregates: implication in a loss-of-function pathology.Defining the limits: Protein aggregation and toxicity in vivoDefects in tongue papillae and taste sensation indicate a problem with neurotrophic support in various neurological diseases.Huntington's disease: revisiting the aggregation hypothesis in polyglutamine neurodegenerative diseases.A network of protein interactions determines polyglutamine toxicity.Early changes in cerebellar physiology accompany motor dysfunction in the polyglutamine disease spinocerebellar ataxia type 3Polyglutamine expansion alters the dynamics and molecular architecture of aggregates in dentatorubropallidoluysian atrophyHuntingtin aggregation kinetics and their pathological role in a Drosophila Huntington's disease modelToward understanding Machado-Joseph diseaseAberrant histone acetylation, altered transcription, and retinal degeneration in a Drosophila model of polyglutamine disease are rescued by CREB-binding proteinA functional deficiency of TERA/VCP/p97 contributes to impaired DNA repair in multiple polyglutamine diseasesEvolution and function of CAG/polyglutamine repeats in protein-protein interaction networks.Conformational switch of polyglutamine-expanded huntingtin into benign aggregates leads to neuroprotective effect.Differential recruitment of UBQLN2 to nuclear inclusions in the polyglutamine diseases HD and SCA3.Structural properties and neuronal toxicity of amyotrophic lateral sclerosis-associated Cu/Zn superoxide dismutase 1 aggregates.Machado-Joseph disease/spinocerebellar ataxia type 3.Single neuron ubiquitin-proteasome dynamics accompanying inclusion body formation in huntington disease.Cytoplasmic retention of polyglutamine-expanded androgen receptor ameliorates disease via autophagy in a mouse model of spinal and bulbar muscular atrophy.Inefficient degradation of truncated polyglutamine proteins by the proteasome.Consensus paper: pathological mechanisms underlying neurodegeneration in spinocerebellar ataxias.Amyloid oligomers: dynamics and toxicity in the cytosol and nucleus.Aggregation of polyglutamine-expanded ataxin-3 sequesters its specific interacting partners into inclusions: implication in a loss-of-function pathology.Modifiers and mechanisms of multi-system polyglutamine neurodegenerative disorders: lessons from fly models.Physical chemistry of polyglutamine: intriguing tales of a monotonous sequence.Protein misfolding in the late-onset neurodegenerative diseases: common themes and the unique case of amyotrophic lateral sclerosis.Targeting specific HATs for neurodegenerative disease treatment: translating basic biology to therapeutic possibilities.
P2860
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P2860
Live-cell imaging reveals divergent intracellular dynamics of polyglutamine disease proteins and supports a sequestration model of pathogenesis.
description
2002 nî lūn-bûn
@nan
2002 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
2002 թվականի հունիսին հրատարակված գիտական հոդված
@hy
2002年の論文
@ja
2002年論文
@yue
2002年論文
@zh-hant
2002年論文
@zh-hk
2002年論文
@zh-mo
2002年論文
@zh-tw
2002年论文
@wuu
name
Live-cell imaging reveals dive ...... stration model of pathogenesis
@nl
Live-cell imaging reveals dive ...... tration model of pathogenesis.
@ast
Live-cell imaging reveals dive ...... tration model of pathogenesis.
@en
Live-cell imaging reveals dive ...... tration model of pathogenesis.
@en-gb
type
label
Live-cell imaging reveals dive ...... stration model of pathogenesis
@nl
Live-cell imaging reveals dive ...... tration model of pathogenesis.
@ast
Live-cell imaging reveals dive ...... tration model of pathogenesis.
@en
Live-cell imaging reveals dive ...... tration model of pathogenesis.
@en-gb
prefLabel
Live-cell imaging reveals dive ...... stration model of pathogenesis
@nl
Live-cell imaging reveals dive ...... tration model of pathogenesis.
@ast
Live-cell imaging reveals dive ...... tration model of pathogenesis.
@en
Live-cell imaging reveals dive ...... tration model of pathogenesis.
@en-gb
P2093
P2860
P356
P1476
Live-cell imaging reveals dive ...... stration model of pathogenesis
@en
P2093
Henry L Paulson
Jianqiang Shao
Victor M Miller
Yaohui Chai
P2860
P304
P356
10.1073/PNAS.152101299
P407
P577
2002-06-25T00:00:00Z