Paradoxical delay in the onset of disease caused by super-long CAG repeat expansions in R6/2 mice.
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Early alterations of brain cellular energy homeostasis in Huntington disease modelsTissue transglutaminase overexpression does not modify the disease phenotype of the R6/2 mouse model of Huntington's diseaseMouse models of polyglutamine diseases: review and data table. Part IEffects of the Pimelic Diphenylamide Histone Deacetylase Inhibitor HDACi 4b on the R6/2 and N171-82Q Mouse Models of Huntington's DiseaseTemporal separation of aggregation and ubiquitination during early inclusion formation in transgenic mice carrying the Huntington's disease mutationOnset and progression of behavioral and molecular phenotypes in a novel congenic R6/2 line exhibiting intergenerational CAG repeat stability.Unusual structures are present in DNA fragments containing super-long Huntingtin CAG repeatsComprehensive behavioral testing in the R6/2 mouse model of Huntington's disease shows no benefit from CoQ10 or minocyclineSystematic behavioral evaluation of Huntington's disease transgenic and knock-in mouse models.Rescuing the Corticostriatal Synaptic Disconnection in the R6/2 Mouse Model of Huntington's Disease: Exercise, Adenosine Receptors and AmpakinesA restricted population of CB1 cannabinoid receptors with neuroprotective activityMonomeric, oligomeric and polymeric proteins in huntington disease and other diseases of polyglutamine expansionGenetic deletion of transglutaminase 2 does not rescue the phenotypic deficits observed in R6/2 and zQ175 mouse models of Huntington's disease.Mitochondrial calcium uptake capacity as a therapeutic target in the R6/2 mouse model of Huntington's disease.Early autophagic response in a novel knock-in model of Huntington diseaseLack of efficacy of NMDA receptor-NR2B selective antagonists in the R6/2 model of Huntington disease.Delayed Onset and Reduced Cognitive Deficits through Pre-Conditioning with 3-Nitropropionic Acid is Dependent on Sex and CAG Repeat Length in the R6/2 Mouse Model of Huntington's Disease.Huntington's disease mouse models online: high-resolution MRI images with stereotaxic templates for computational neuroanatomyAdaptation to experimental jet-lag in R6/2 mice despite circadian dysrhythmia.Mechanisms of trinucleotide repeat instability during human developmentDisruption of the nuclear membrane by perinuclear inclusions of mutant huntingtin causes cell-cycle re-entry and striatal cell death in mouse and cell models of Huntington's disease.A critical window of CAG repeat-length correlates with phenotype severity in the R6/2 mouse model of Huntington's disease.Comparison of mHTT Antibodies in Huntington's Disease Mouse Models Reveal Specific Binding Profiles and Steady-State Ubiquitin Levels with Disease DevelopmentThe group 2 metabotropic glutamate receptor agonist LY379268 rescues neuronal, neurochemical and motor abnormalities in R6/2 Huntington's disease miceAllelic series of Huntington's disease knock-in mice reveals expression discorrelates.Aggregation formation in the polyglutamine diseases: protection at a cost?Mitochondrial permeability transition pore induces mitochondria injury in Huntington disease.Potential molecular consequences of transgene integration: The R6/2 mouse example.Right ventricular dysfunction in the R6/2 transgenic mouse model of Huntington's disease is unmasked by dobutamineHuntington's disease: can mice lead the way to treatment?Huntingtin-lowering strategies in Huntington's disease: antisense oligonucleotides, small RNAs, and gene editing.Animal models of Huntington's disease for translation to the clinic: best practices.Polyglutamine Aggregation in Huntington Disease: Does Structure Determine Toxicity?Targeting CAG repeat RNAs reduces Huntington's disease phenotype independently of huntingtin levels.Similar Progression of Morphological and Metabolic Phenotype in R6/2 Mice with Different CAG Repeats Revealed by In Vivo Magnetic Resonance Imaging and Spectroscopy.A multifunctional, multi-pathway intracellular localization signal in Huntingtin.Evidence from the R6/2 Mouse Model of Huntington's Disease for Using Abnormal Brain Metabolism as a Biomarker for Evaluating Therapeutic Approaches for TreatmentRestriction endonuclease TseI cleaves A:A and T:T mismatches in CAG and CTG repeats.Voxel-based morphometry with templates and validation in a mouse model of Huntington's disease.Ghrelin rescues skeletal muscle catabolic profile in the R6/2 mouse model of Huntington's disease
P2860
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P2860
Paradoxical delay in the onset of disease caused by super-long CAG repeat expansions in R6/2 mice.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
@yue
2008年學術文章
@zh-hant
name
Paradoxical delay in the onset ...... epeat expansions in R6/2 mice.
@en
Paradoxical delay in the onset ...... epeat expansions in R6/2 mice.
@nl
type
label
Paradoxical delay in the onset ...... epeat expansions in R6/2 mice.
@en
Paradoxical delay in the onset ...... epeat expansions in R6/2 mice.
@nl
prefLabel
Paradoxical delay in the onset ...... epeat expansions in R6/2 mice.
@en
Paradoxical delay in the onset ...... epeat expansions in R6/2 mice.
@nl
P2093
P1476
Paradoxical delay in the onset ...... repeat expansions in R6/2 mice
@en
P2093
Dervila Glynn
James M Wight
Jeremy N Skepper
Wendy Leavens
Zhiguang Zheng
P304
P356
10.1016/J.NBD.2008.11.015
P577
2008-12-11T00:00:00Z