CHIP protects from the neurotoxicity of expanded and wild-type ataxin-1 and promotes their ubiquitination and degradation
about
Phenotype and frequency of STUB1 mutations: next-generation screenings in Caucasian ataxia and spastic paraplegia cohortsThe ataxia protein sacsin is a functional co-chaperone that protects against polyglutamine-expanded ataxin-1Animal models of polyglutamine diseases and therapeutic approachesModel systems of protein-misfolding diseases reveal chaperone modifiers of proteotoxicityTargeting heat shock proteins to modulate α-synuclein toxicityBeyond the glutamine expansion: influence of posttranslational modifications of ataxin-1 in the pathogenesis of spinocerebellar ataxia type 1dAtaxin-2 mediates expanded Ataxin-1-induced neurodegeneration in a Drosophila model of SCA1A Decade of Boon or Burden: What Has the CHIP Ever Done for Cellular Protein Quality Control Mechanism Implicated in Neurodegeneration and Aging?E2-25K/Hip-2 regulates caspase-12 in ER stress-mediated Abeta neurotoxicityIdentification of CHIP as a novel causative gene for autosomal recessive cerebellar ataxiaAtaxia and hypogonadism caused by the loss of ubiquitin ligase activity of the U box protein CHIPA critical role for CHIP in the aggresome pathwayRegulation of LRRK2 stability by the E3 ubiquitin ligase CHIPUbiquitinylation of α-synuclein by carboxyl terminus Hsp70-interacting protein (CHIP) is regulated by Bcl-2-associated athanogene 5 (BAG5).Inhibition of hsp70 by methylene blue affects signaling protein function and ubiquitination and modulates polyglutamine protein degradationHeat shock protein 70 (hsp70) as an emerging drug target.The ubiquitin-proteasome system in neurodegenerative diseases: precipitating factor, yet part of the solutionNeurodegenerative models in Drosophila: polyglutamine disorders, Parkinson disease, and amyotrophic lateral sclerosis.Correlation of inter-locus polyglutamine toxicity with CAG•CTG triplet repeat expandability and flanking genomic DNA GC contentIdentification of common genetic modifiers of neurodegenerative diseases from an integrative analysis of diverse genetic screens in model organismsInhibition of lipid signaling enzyme diacylglycerol kinase epsilon attenuates mutant huntingtin toxicity.STUB1 mutations in autosomal recessive ataxias - evidence for mutation-specific clinical heterogeneity.The vasculome of the mouse brain.Pathogenic polyglutamine expansion length correlates with polarity of the flanking sequences.Proposal for a role of the Hsp90/Hsp70-based chaperone machinery in making triage decisions when proteins undergo oxidative and toxic damage.Neuronal store-operated calcium entry pathway as a novel therapeutic target for Huntington's disease treatment.Focused cerebellar laser light induced hyperthermia improves symptoms and pathology of polyglutamine disease SCA1 in a mouse model.A striatal-enriched intronic GPCR modulates huntingtin levels and toxicityMolecular and functional characterization of the only known hemiascomycete ortholog of the carboxyl terminus of Hsc70-interacting protein CHIP in the yeast Yarrowia lipolytica.Post-translational modifications of nuclear receptors and human diseasePolyunsaturated fatty acids induce alpha-synuclein-related pathogenic changes in neuronal cellsEnhancement of ubiquitin conjugation activity reduces intracellular aggregation of V76D mutant γD-crystallin.Phosphorylation of CHIP at Ser20 by Cdk5 promotes tAIF-mediated neuronal death.Identification of novel genes that modify phenotypes induced by Alzheimer's beta-amyloid overexpression in DrosophilaEmerging evidence of coding mutations in the ubiquitin-proteasome system associated with cerebellar ataxiasSex-dependent effect of BAG1 in ameliorating motor deficits of Huntington disease transgenic mice.Novel therapeutic strategies for the treatment of protein-misfolding diseases.Protein quality control and degradation in cardiomyocytes.Polyglutamine neurodegeneration: protein misfolding revisited.CHIP deletion reveals functional redundancy of E3 ligases in promoting degradation of both signaling proteins and expanded glutamine proteins
P2860
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P2860
CHIP protects from the neurotoxicity of expanded and wild-type ataxin-1 and promotes their ubiquitination and degradation
description
2006 nî lūn-bûn
@nan
2006 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2006 թվականի սեպտեմբերին 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
CHIP protects from the neuroto ...... ubiquitination and degradation
@ast
CHIP protects from the neuroto ...... ubiquitination and degradation
@en
CHIP protects from the neuroto ...... ubiquitination and degradation
@en-gb
CHIP protects from the neuroto ...... ubiquitination and degradation
@nl
type
label
CHIP protects from the neuroto ...... ubiquitination and degradation
@ast
CHIP protects from the neuroto ...... ubiquitination and degradation
@en
CHIP protects from the neuroto ...... ubiquitination and degradation
@en-gb
CHIP protects from the neuroto ...... ubiquitination and degradation
@nl
prefLabel
CHIP protects from the neuroto ...... ubiquitination and degradation
@ast
CHIP protects from the neuroto ...... ubiquitination and degradation
@en
CHIP protects from the neuroto ...... ubiquitination and degradation
@en-gb
CHIP protects from the neuroto ...... ubiquitination and degradation
@nl
P2093
P2860
P50
P921
P3181
P356
P1476
CHIP protects from the neuroto ...... ubiquitination and degradation
@en
P2093
Alma M Pérez
Beatrice de Gouyon
Hung-Kai Chen
Ismael Al-Ramahi
Joana Branco
Juan Botas
Minghang Zhang
Yung C Lam
P2860
P304
P3181
P356
10.1074/JBC.M601603200
P407
P577
2006-09-08T00:00:00Z