Caspase 3-cleaved N-terminal fragments of wild-type and mutant huntingtin are present in normal and Huntington's disease brains, associate with membranes, and undergo calpain-dependent proteolysis.
about
Oligonucleotide therapeutic approaches for Huntington diseaseHuntingtin and huntingtin-associated protein 1 influence neuronal calcium signaling mediated by inositol-(1,4,5) triphosphate receptor type 1CDK5 protects from caspase-induced Ataxin-3 cleavage and neurodegenerationThe predominantly HEAT-like motif structure of huntingtin and its association and coincident nuclear entry with dorsal, an NF-kB/Rel/dorsal family transcription factorIron dysregulation in Huntington's diseaseTransgenic animal models for study of the pathogenesis of Huntington's disease and therapyRole of apoptosis in diseasePathogenic mechanisms and therapeutic strategies in spinobulbar muscular atrophyTherapeutic 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 crystal structure of caspase-6, a selective effector of axonal degenerationRole of NMDA Receptor-Mediated Glutamatergic Signaling in Chronic and Acute NeuropathologiesPhosphorylation of arfaptin 2 at Ser260 by Akt Inhibits PolyQ-huntingtin-induced toxicity by rescuing proteasome impairmentCalpain and STriatal-Enriched protein tyrosine phosphatase (STEP) activation contribute to extrasynaptic NMDA receptor localization in a Huntington's disease mouse modelNormal huntingtin function: an alternative approach to Huntington's diseaseInhibition of calpain cleavage of huntingtin reduces toxicity: accumulation of calpain/caspase fragments in the nucleusMutant huntingtin alters cell fate in response to microtubule depolymerization via the GEF-H1-RhoA-ERK pathwayNuclear localization of a non-caspase truncation product of atrophin-1, with an expanded polyglutamine repeat, increases cellular toxicityIdentification of a karyopherin β1/β2 proline-tyrosine nuclear localization signal in huntingtin protein.N-terminal mutant huntingtin associates with mitochondria and impairs mitochondrial trafficking.SCA1-like disease in mice expressing wild-type ataxin-1 with a serine to aspartic acid replacement at residue 776.Identification of a post-translationally myristoylated autophagy-inducing domain released by caspase cleavage of huntingtin.Cholesterol Modifies Huntingtin Binding to, Disruption of, and Aggregation on Lipid Membranes.Free-Energy Landscape of the Amino-Terminal Fragment of Huntingtin in Aqueous SolutionInteraction of huntingtin fragments with brain membranes--clues to early dysfunction in Huntington's disease.Huntingtin phosphorylation sites mapped by mass spectrometry. Modulation of cleavage and toxicity.Molecular pathogenesis and cellular pathology of spinocerebellar ataxia type 7 neurodegenerationIKKalpha and IKKbeta regulation of DNA damage-induced cleavage of huntingtin.The regulation of N-terminal Huntingtin (Htt552) accumulation by Beclin1.Proteolysis of mutant huntingtin produces an exon 1 fragment that accumulates as an aggregated protein in neuronal nuclei in Huntington disease.Alterations in STriatal-Enriched protein tyrosine Phosphatase expression, activation, and downstream signaling in early and late stages of the YAC128 Huntington's disease mouse model.Monomeric, oligomeric and polymeric proteins in huntington disease and other diseases of polyglutamine expansionA two-step path to inclusion formation of huntingtin peptides revealed by number and brightness analysis.Pathological accumulation of atrophin-1 in dentatorubralpallidoluysian atrophy.Caspase-6 does not contribute to the proteolysis of mutant huntingtin in the HdhQ150 knock-in mouse model of Huntington's diseaseFrom Alzheimer to Huntington: why is a structural understanding so difficult?PROSPER: an integrated feature-based tool for predicting protease substrate cleavage sites.A compact beta model of huntingtin toxicity.Cerebellar soluble mutant ataxin-3 level decreases during disease progression in Spinocerebellar Ataxia Type 3 miceViral delivery of glial cell line-derived neurotrophic factor improves behavior and protects striatal neurons in a mouse model of Huntington's disease
P2860
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P2860
Caspase 3-cleaved N-terminal fragments of wild-type and mutant huntingtin are present in normal and Huntington's disease brains, associate with membranes, and undergo calpain-dependent proteolysis.
description
2001 nî lūn-bûn
@nan
2001 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
2001年の論文
@ja
2001年論文
@yue
2001年論文
@zh-hant
2001年論文
@zh-hk
2001年論文
@zh-mo
2001年論文
@zh-tw
2001年论文
@wuu
name
Caspase 3-cleaved N-terminal f ...... calpain-dependent proteolysis.
@ast
Caspase 3-cleaved N-terminal f ...... calpain-dependent proteolysis.
@en
type
label
Caspase 3-cleaved N-terminal f ...... calpain-dependent proteolysis.
@ast
Caspase 3-cleaved N-terminal f ...... calpain-dependent proteolysis.
@en
prefLabel
Caspase 3-cleaved N-terminal f ...... calpain-dependent proteolysis.
@ast
Caspase 3-cleaved N-terminal f ...... calpain-dependent proteolysis.
@en
P2093
P2860
P356
P1476
Caspase 3-cleaved N-terminal f ...... calpain-dependent proteolysis
@en
P2093
M DiFiglia
P2860
P304
12784-12789
P356
10.1073/PNAS.221451398
P407
P50
P577
2001-10-01T00:00:00Z