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Expression data from striatum of a mouse model of Huntington´s disease (HD) (HdhQ111/Q111) crossed with mGluR5 knockout mice (mGluR5-/-) and their respective controls (HdhQ20/Q20 and mGluR5+/+).

ABSTRACT: To try to investigate the mechanism behind the adaptive phenotypes observed in a mice model model of HD crossed with mGluR5 knockout, we analyzed whether mutated huntingtin (Htt) expression in a mGluR5 null background could be altering the expression of genes that might be involved in the pattern of Htt aggregation and HD-related locomotor alterations. In this data set, we include analysis of gene expression in striatum of mice with four different genotypes: HdhQ20/Q20/mGluR5+/+; HdhQ20/Q20/mGluR5-/- ; HdhQ111/Q111/mGluR5+/+ ; HdhQ111/Q111/mGluR5-/-

ORGANISM(S): Mus musculus

PROVIDER: GSE50379 | GEO | 2013/08/28

SECONDARY ACCESSION(S): PRJNA217365

REPOSITORIES: GEO

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Expression data from striatum of a mouse model of Huntington´s disease (HD) (HdhQ111/Q111) crossed with mGluR5 knockout mice (mGluR5-/-) and their respective controls (HdhQ20/Q20 and mGluR5+/+).

Project description:To try to investigate the mechanism behind the adaptive phenotypes observed in a mice model model of HD crossed with mGluR5 knockout, we analyzed whether mutated huntingtin (Htt) expression in a mGluR5 null background could be altering the expression of genes that might be involved in the pattern of Htt aggregation and HD-related locomotor alterations. In this data set, we include analysis of gene expression in striatum of mice with four different genotypes: HdhQ20/Q20/mGluR5+/+; HdhQ20/Q20/mGluR5-/- ; HdhQ111/Q111/mGluR5+/+ ; HdhQ111/Q111/mGluR5-/- 12 samples were analyzed. We used Partek Genomics Suite v6.5 (Partek, St. Louis, MO) to determine differences in gene expression levels. Genotype effects were considered significant based of the following criteria: (i) ANOVA p-values< 0.05 and (ii) 1.5 fold increase or decrease.

2013-08-28 | E-GEOD-50379 | biostudies-arrayexpress

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Project description:Transcriptional changes are an early feature of Huntington's disease (HD). We profiled genome-wide interaction sites for the huntingtin protein (HTT) using ChIP-sequencing from mouse striatal tissue at 4 months of age. We include replicate samples from CAG-expanded murine Htt (heterozygous Q111/+) and wildtype littermate controls.

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Project description:Although Huntington’s disease (HD) is a late onset neurological condition, studies suggest a developmental contribution to its adult manifestations. Imaging studies in presymptomatic HD gene carriers revealed early alterations in white matter tract with a marked defect in the corpus callosum. This tract is mainly formed by axons projecting from layer II/III neurons. HD leads to microtubule bundling defects in the growth cone, the cellular compartment that drives axonal growth. We performed a mass spectrometry-based proteomic analysis of growth cones from WT (HdhQ7/Q7) and HD (HdhQ7/Q111) mice to identify proteins involved in HD-induced phenotypes on axonal growth and on the growth cone microtubule cytoskeleton.

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Mus musculus

Project description:Expression data from striatum of a mouse model of Huntington´s disease (HD) (HdhQ111/Q111) crossed with mGluR5 knockout mice (mGluR5-/-) and their respective controls (HdhQ20/Q20 and mGluR5+/+).

| PRJNA217365 | ENA

Expression data from a cell model of Huntington disease

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Expression analysis in yeast model of Huntington's disease (HD)

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Project description:Expressing a mutant fragment of huntingtin (Htt) in yeast produces several HD-relevant phenotypes. We used microarrays to study global change in expression induced by this mutant htt fragment. Expression was also analysed in three suppressor deletion strains expressing a toxic mutant htt fragment: bna4Δ, mbf1Δ, and ume1Δ. Yeast samples expressing either a wild-type or mutant htt fragment (Htt25Q or Htt103Q, respectively), and suppressor deletion strains expressing Htt103Q: bna4Δ, mbf1Δ, and ume1Δ.

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Project description:To identify genes affected by mutant huntington protein, we performed mRNA-seq experiments with Striatal STHdh Q7/Q7, Q7Q111, and Q111/Q111 cells. We also tested the effect of Sp1 overexpression on rescuing gene expression in Q111/Q111 cells.

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Specificity assessment of allele selective Zinc Finger Protein Repressors in HD fibroblasts

Project description:Huntington’s disease (HD) is a dominantly inherited neurodegenerative disorder caused by a CAG trinucleotide expansion in the huntingtin gene (HTT), which codes for the pathologic mutant HTT (mHTT) protein. Since normal HTT is thought to be important for brain function, we engineered zinc finger protein transcription factors (ZFP-TFs) to target the pathogenic CAG repeat and selectively lower mHTT as a therapeutic strategy. Using patient-derived fibroblasts and neurons, we demonstrate that ZFP-TFs selectively repress >99% of HD-causing alleles over a wide dose range, while preserving expression of >86% of normal alleles. Other CAG-containing genes are minimally affected, and virally delivered ZFP-TFs are active and well tolerated in HD neurons beyond 100 days in culture and at least 9 months in the mouse brain. Using three HD mouse models, we demonstrate improvements in a range of molecular, histopathological, electrophysiological, and functional endpoints. Our findings support the continued development of an allele-selective ZFP-TF for the treatment of HD.

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