Inhibiting caspase cleavage of huntingtin reduces toxicity and aggregate formation in neuronal and nonneuronal cells.
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Huntingtin interacting protein 1 induces apoptosis via a novel caspase-dependent death effector domainHuntingtin and huntingtin-associated protein 1 influence neuronal calcium signaling mediated by inositol-(1,4,5) triphosphate receptor type 1SATB1 cleavage by caspase 6 disrupts PDZ domain-mediated dimerization, causing detachment from chromatin early in T-cell apoptosisAccurate prediction of the functional significance of single nucleotide polymorphisms and mutations in the ABCA1 geneTransgenic animal models for study of the pathogenesis of Huntington's disease and therapyTherapeutic 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 degenerationSubstrate-Induced Conformational Changes Occur in All Cleaved Forms of Caspase-6Huntingtin functions as a scaffold for selective macroautophagyPhosphorylation of arfaptin 2 at Ser260 by Akt Inhibits PolyQ-huntingtin-induced toxicity by rescuing proteasome impairmentStructure, binding interface and hydrophobic transitions of Ca2+-loaded calbindin-D(28K)Normal 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 pathwayA quantitative method for the specific assessment of caspase-6 activity in cell cultureMice lacking caspase-2 are protected from behavioral changes, but not pathology, in the YAC128 model of Huntington disease.Transgenic mice expressing caspase-6-derived N-terminal fragments of mutant huntingtin develop neurologic abnormalities with predominant cytoplasmic inclusion pathology composed largely of a smaller proteolytic derivative.Identification of a post-translationally myristoylated autophagy-inducing domain released by caspase cleavage of huntingtin.Calpain inhibition mediates autophagy-dependent protection against polyglutamine toxicity.Caspase vinyl sulfone small molecule inhibitors prevent axonal degeneration in human neurons and reverse cognitive impairment in Caspase-6-overexpressing mice.Huntingtin phosphorylation sites mapped by mass spectrometry. Modulation of cleavage and toxicity.Molecular pathogenesis and cellular pathology of spinocerebellar ataxia type 7 neurodegenerationF-actin binding regions on the androgen receptor and huntingtin increase aggregation and alter aggregate characteristicsPolyglutamine-rich suppressors of huntingtin toxicity act upstream of Hsp70 and Sti1 in spatial quality control of amyloid-like proteins.Effect of post-mortem delay on N-terminal huntingtin protein fragments in human control and Huntington disease brain lysates.Identification and evaluation of small molecule pan-caspase inhibitors in Huntington's disease models.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.Expanded polyglutamines in Caenorhabditis elegans cause axonal abnormalities and severe dysfunction of PLM mechanosensory neurons without cell deathWild-type huntingtin reduces the cellular toxicity of mutant huntingtin in vivoTauroursodeoxycholic acid, a bile acid, is neuroprotective in a transgenic animal model of Huntington's disease.Nitric oxide and nitric oxide synthase in Huntington's disease.The selective vulnerability of nerve cells in Huntington's disease.Therapeutic approaches to preventing cell death in Huntington diseaseThe common inhaled anesthetic isoflurane increases aggregation of huntingtin and alters calcium homeostasis in a cell model of Huntington's diseaseProtein aggregates and dementia: is there a common toxicity?Analysis of proteolytic processes and enzymatic activities in the generation of huntingtin n-terminal fragments in an HEK293 cell model.Mitochondrial fission and cristae disruption increase the response of cell models of Huntington's disease to apoptotic stimuli.Cysteine proteases bleomycin hydrolase and cathepsin Z mediate N-terminal proteolysis and toxicity of mutant huntingtin.Cleavage at the 586 amino acid caspase-6 site in mutant huntingtin influences caspase-6 activation in vivo.
P2860
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P2860
Inhibiting caspase cleavage of huntingtin reduces toxicity and aggregate formation in neuronal and nonneuronal cells.
description
2000 nî lūn-bûn
@nan
2000年の論文
@ja
2000年学术文章
@wuu
2000年学术文章
@zh-cn
2000年学术文章
@zh-hans
2000年学术文章
@zh-my
2000年学术文章
@zh-sg
2000年學術文章
@yue
2000年學術文章
@zh
2000年學術文章
@zh-hant
name
Inhibiting caspase cleavage of ...... euronal and nonneuronal cells.
@en
type
label
Inhibiting caspase cleavage of ...... euronal and nonneuronal cells.
@en
prefLabel
Inhibiting caspase cleavage of ...... euronal and nonneuronal cells.
@en
P2093
P356
P1476
Inhibiting caspase cleavage of ...... euronal and nonneuronal cells.
@en
P2093
C L Wellington
D E Bredesen
D W Nicholson
N Thornberry
R Singaraja
P304
19831-19838
P356
10.1074/JBC.M001475200
P407
P577
2000-06-01T00:00:00Z