Huntingtin inclusion bodies are iron-dependent centers of oxidative events.
about
Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson's, Huntington's, Alzheimer's, prions, bactericides, chemical toxicology and others as examplesThe choreography of neuroinflammation in Huntington's diseaseIron dysregulation in Huntington's diseaseExperimental and computational analysis of polyglutamine-mediated cytotoxicityRole of oxidative DNA damage in mitochondrial dysfunction and Huntington's disease pathogenesisMetabolism in HD: still a relevant mechanism?Role of iron in neurodegenerative diseases.Mechanisms of copper ion mediated Huntington's disease progressionConformational targeting of fibrillar polyglutamine proteins in live cells escalates aggregation and cytotoxicity.Altered manganese homeostasis and manganese toxicity in a Huntington's disease striatal cell model are not explained by defects in the iron transport system.Expanded ataxin-7 cause toxicity by inducing ROS production from NADPH oxidase complexes in a stable inducible Spinocerebellar ataxia type 7 (SCA7) model.Iron accumulates in Huntington's disease neurons: protection by deferoxamineHsp27 (HspB1) and alphaB-crystallin (HspB5) as therapeutic targets.Novel therapeutic strategies for the treatment of protein-misfolding diseases.Neonatal Iron Supplementation Induces Striatal Atrophy in Female YAC128 Huntington's Disease Mice.Abnormal iron homeostasis and neurodegeneration.Cytochrome c-mediated oxidation of hydroethidine and mito-hydroethidine in mitochondria: identification of homo- and heterodimersPathology-dependent effects linked to small heat shock proteins expression: an updateMitochondrial DNA damage is associated with reduced mitochondrial bioenergetics in Huntington's disease.The iron regulatory capability of the major protein participants in prevalent neurodegenerative disorders.Role of manganese in neurodegenerative diseases.Protein oxidation in Huntington disease.Energy dysfunction in Huntington's disease: insights from PGC-1α, AMPK, and CKB.HPLC-based monitoring of products formed from hydroethidine-based fluorogenic probes--the ultimate approach for intra- and extracellular superoxide detection.Connectivity mapping uncovers small molecules that modulate neurodegeneration in Huntington's disease models.hMTH1 expression protects mitochondria from Huntington's disease-like impairment.In vitro and in vivo aggregation of a fragment of huntingtin protein directly causes free radical production.GFP-LC3 labels organised smooth endoplasmic reticulum membranes independently of autophagy.Protein aggregation into insoluble deposits protects from oxidative stress.Antioxidants cannot suppress the lethal phenotype of a Drosophila melanogaster model of Huntington's disease.Glyceraldehyde 3-phosphate dehydrogenase augments the intercellular transmission and toxicity of polyglutamine aggregates in a cell model of Huntington disease.Amyloid Precursor Protein Haploinsufficiency Preferentially Mediates Brain Iron Accumulation in Mice Transgenic for The Huntington's Disease Mutation.Mutant huntingtin induces iron overload via up-regulating IRP1 in Huntington's disease.
P2860
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P2860
Huntingtin inclusion bodies are iron-dependent centers of oxidative events.
description
2006 nî lūn-bûn
@nan
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
2006年论文
@zh
2006年论文
@zh-cn
name
Huntingtin inclusion bodies are iron-dependent centers of oxidative events.
@en
type
label
Huntingtin inclusion bodies are iron-dependent centers of oxidative events.
@en
prefLabel
Huntingtin inclusion bodies are iron-dependent centers of oxidative events.
@en
P2093
P2860
P1433
P1476
Huntingtin inclusion bodies are iron-dependent centers of oxidative events
@en
P2093
Andreas Wyttenbach
André-Patrick Arrigo
Paola Giuliano
R William Currie
Wance J J Firdaus
P2860
P304
P356
10.1111/J.1742-4658.2006.05537.X
P407
P50
P577
2006-12-01T00:00:00Z