Mutant huntingtin fragment selectively suppresses Brn-2 POU domain transcription factor to mediate hypothalamic cell dysfunction
about
Maintenance of basal levels of autophagy in Huntington's disease mouse models displaying metabolic dysfunctionLoss of aPKCλ in differentiated neurons disrupts the polarity complex but does not induce obvious neuronal loss or disorientation in mouse brainsProteomic screening for amyloid proteinsAn aggregation sensing reporter identifies leflunomide and teriflunomide as polyglutamine aggregate inhibitors.Polyglutamine toxicity is controlled by prion composition and gene dosage in yeast.Genome-wide prediction and analysis of human tissue-selective genes using microarray expression dataLarge-scale RNA interference screening in mammalian cells identifies novel regulators of mutant huntingtin aggregation.Metabolic and behavioral effects of mutant huntingtin deletion in Sim1 neurons in the BACHD mouse model of Huntington's disease.POU-III transcription factors (Brn1, Brn2, and Oct6) influence neurogenesis, molecular identity, and migratory destination of upper-layer cells of the cerebral cortexDifferential roles of NF-Y transcription factor in ER chaperone expression and neuronal maintenance in the CNSAssociation of the PDYN gene with alcohol dependence and the propensity to drink in negative emotional states.Hypothalamic alterations in Huntington's disease patients: comparison with genetic rodent models.Genome-wide analyses in neuronal cells reveal that upstream transcription factors regulate lysosomal gene expression.NF-Y inactivation causes atypical neurodegeneration characterized by ubiquitin and p62 accumulation and endoplasmic reticulum disorganization.Could yeast prion domains originate from polyQ/N tracts?Depletion of p62 reduces nuclear inclusions and paradoxically ameliorates disease phenotypes in Huntington's model mice.Biodegradable delivery system containing a peptide inhibitor of polyglutamine aggregation: a step toward therapeutic development in Huntington's disease.Functional increase of brain histaminergic signaling in Huntington's disease.Heat shock factor-1 influences pathological lesion distribution of polyglutamine-induced neurodegeneration.Hypothalamic Alterations in Neurodegenerative Diseases and Their Relation to Abnormal Energy Metabolism.
P2860
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P2860
Mutant huntingtin fragment selectively suppresses Brn-2 POU domain transcription factor to mediate hypothalamic cell dysfunction
description
2010 nî lūn-bûn
@nan
2010年の論文
@ja
2010年学术文章
@wuu
2010年学术文章
@zh-cn
2010年学术文章
@zh-hans
2010年学术文章
@zh-my
2010年学术文章
@zh-sg
2010年學術文章
@yue
2010年學術文章
@zh
2010年學術文章
@zh-hant
name
Mutant huntingtin fragment sel ...... hypothalamic cell dysfunction
@en
type
label
Mutant huntingtin fragment sel ...... hypothalamic cell dysfunction
@en
prefLabel
Mutant huntingtin fragment sel ...... hypothalamic cell dysfunction
@en
P2093
P2860
P356
P1476
Mutant huntingtin fragment sel ...... hypothalamic cell dysfunction
@en
P2093
Asako Tosaki
Haruko Miyazaki
Masaru Kurosawa
Mizuki Yamada
Nobuyuki Nukina
Tomoyuki Yamanaka
P2860
P304
P356
10.1093/HMG/DDQ087
P577
2010-02-25T00:00:00Z