about
HDAC4 reduction: a novel therapeutic strategy to target cytoplasmic huntingtin and ameliorate neurodegenerationDiminished hippocalcin expression in Huntington's disease brain does not account for increased striatal neuron vulnerability as assessed in primary neuronsSIRT2 inhibition achieves neuroprotection by decreasing sterol biosynthesisDecreased striatal RGS2 expression is neuroprotective in Huntington's disease (HD) and exemplifies a compensatory aspect of HD-induced gene regulationHDAC4 does not act as a protein deacetylase in the postnatal murine brain in vivoInvolvement of autophagy in hypoxic-excitotoxic neuronal deathSynchrotron infrared microspectroscopy detecting the evolution of Huntington's disease neuropathology and suggesting unique correlates of dysfunction in white versus gray brain matter.Altered chromatin architecture underlies progressive impairment of the heat shock response in mouse models of Huntington disease.Expression analysis of novel striatal-enriched genes in Huntington disease.Assessment of the relationship between pre-chip and post-chip quality measures for Affymetrix GeneChip expression data.Analysis of potential transcriptomic biomarkers for Huntington's disease in peripheral blood.A potent and selective Sirtuin 1 inhibitor alleviates pathology in multiple animal and cell models of Huntington's disease.Computational deconvolution of genome wide expression data from Parkinson's and Huntington's disease brain tissues using population-specific expression analysis.Transcriptional dysregulation in striatal projection- and interneurons in a mouse model of Huntington's disease: neuronal selectivity and potential neuroprotective role of HAP1.Regional and cellular gene expression changes in human Huntington's disease brain.Cross-species and cross-platform gene expression studies with the Bioconductor-compliant R package 'annotationTools'Short-term striatal gene expression responses to brain-derived neurotrophic factor are dependent on MEK and ERK activation.Decreased Lin7b expression in layer 5 pyramidal neurons may contribute to impaired corticostriatal connectivity in huntington disease.Transcriptional changes in Huntington disease identified using genome-wide expression profiling and cross-platform analysisA brain-permeable small molecule reduces neuronal cholesterol by inhibiting activity of sirtuin 2 deacetylase.Genome-wide histone acetylation is altered in a transgenic mouse model of Huntington's disease.Comparative analyses of Purkinje cell gene expression profiles reveal shared molecular abnormalities in models of different polyglutamine diseases.An adeno-associated virus-based intracellular sensor of pathological nuclear factor-κB activation for disease-inducible gene transfer.MicroRNA-22 (miR-22) overexpression is neuroprotective via general anti-apoptotic effects and may also target specific Huntington's disease-related mechanismsIn vivo cell-autonomous transcriptional abnormalities revealed in mice expressing mutant huntingtin in striatal but not cortical neurons.MAP kinase phosphatase 1 (MKP-1/DUSP1) is neuroprotective in Huntington's disease via additive effects of JNK and p38 inhibitionA large number of protein expression changes occur early in life and precede phenotype onset in a mouse model for huntington disease.Calpain hydrolysis of alpha- and beta2-adaptins decreases clathrin-dependent endocytosis and may promote neurodegeneration.What have we learned from gene expression profiles in Huntington's disease?Genome-wide increase in histone H2A ubiquitylation in a mouse model of Huntington's disease.Increased huntingtin protein length reduces the number of polyglutamine-induced gene expression changes in mouse models of Huntington's disease.Polyglutamine and transcription: gene expression changes shared by DRPLA and Huntington's disease mouse models reveal context-independent effects.Connectivity mapping uncovers small molecules that modulate neurodegeneration in Huntington's disease models.Sustained effects of nonallele-specific Huntingtin silencing.The ratio of monomeric to aggregated forms of Abeta40 and Abeta42 is an important determinant of amyloid-beta aggregation, fibrillogenesis, and toxicity.Neuroprotective role of Sirt1 in mammalian models of Huntington's disease through activation of multiple Sirt1 targets.Cell loss in the motor and cingulate cortex correlates with symptomatology in Huntington's disease.Mutant huntingtin's effects on striatal gene expression in mice recapitulate changes observed in human Huntington's disease brain and do not differ with mutant huntingtin length or wild-type huntingtin dosage.Differential D1 and D2 receptor-mediated effects on immediate early gene induction in a transgenic mouse model of Huntington's disease.Gene expression profiling of R6/2 transgenic mice with different CAG repeat lengths reveals genes associated with disease onset and progression in Huntington's disease.
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description
hulumtuese
@sq
onderzoeker
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researcher
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հետազոտող
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name
Ruth Luthi-Carter
@ast
Ruth Luthi-Carter
@en
Ruth Luthi-Carter
@es
Ruth Luthi-Carter
@nl
type
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Ruth Luthi-Carter
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Ruth Luthi-Carter
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Ruth Luthi-Carter
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Ruth Luthi-Carter
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prefLabel
Ruth Luthi-Carter
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Ruth Luthi-Carter
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Ruth Luthi-Carter
@es
Ruth Luthi-Carter
@nl
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P21
P31
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0000-0002-6827-4273