GEO DataSets

(Submitter supplied) Purpose:The goals of this study was to determine alterations in expression levels of transcripts downstream of a dominant-negative transcription factor. Quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods was used to confirm the altered expression of targets. Methods: Striatal mRNA profiles of 11-month-old wild-type (WT) and Nestin-Cre X PPAR delta E411P mice were generated by deep sequencing, in triplicate, using Illumina HiSeq 2000. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

6 Samples

Download data: TXT

(Submitter supplied) Huntington’s disease (HD), caused by a CAG repeat expansion in the huntingtin (HTT) gene, is characterized by abnormal protein aggregates and motor and cognitive dysfunction. Htt protein is ubiquitously expressed, but the striatal medium spiny neuron (MSN) is most susceptible to neuronal dysfunction and death. Abnormal gene expression represents a core pathogenic feature of HD, but the relative roles of cell-autonomous and non-cell-autonomous effects on transcription remain unclear. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6885

7 Samples

Download data: TXT

(Submitter supplied) Huntington’s Disease (HD) is an inherited neurodegenerative disease caused by a glutamine repeat expansion in huntingtin protein. Transcriptional deregulation and altered energy metabolism have been implicated in HD pathogenesis. We report here that mutant huntingtin causes disruption of mitochondrial function by inhibiting expression of PGC-1a, a transcriptional coactivator that regulates several metabolic processes including mitochondrial biogenesis and respiration. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS2391

Platform:

GPL1261

6 Samples

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Analysis of brain striatum of PGC-1alpha transcriptional coactivator null mutants. PGC-1alpha regulates several metabolic processes. Altered energy metabolism is implicated in Huntington's disease (HD). Results provide insight into the role of PGC-1alpha in HD pathogenesis.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 genotype/variation sets

Platform:

GPL1261

Series:

GSE5786

6 Samples

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(Submitter supplied) Huntington disease (HD) is a fatal neurodegenerative disorder without cure, caused by an aberrant expansion of CAG repeats in the exon 1 of the Huntingtin (HTT) gene. Although the negative correlation between the number of CAG repeats and the age of disease onset is well established, additional factors may contribute to the high heterogeneity in the complex manifestation of the symptoms among patients. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

16 Samples

Download data: TXT

(Submitter supplied) The role of Twist1 in mutant huntingtin-induced transcriptional alterations

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21493

16 Samples

Download data: TXT

(Submitter supplied) Transcriptional dysregulation in a primary cortical neuron model of Huntington's disease

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

12 Samples

Download data: TXT

(Submitter supplied) We report the gene expression alterations observed in freshly isolated microglia from the striatum 10-month-old Q175 mice with and without Tyrobp

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

18 Samples

Download data: TXT

(Submitter supplied) We report the gene expression alterations observed in the striatum 10-month-old Q175 mice with and without Tyrobp

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

24 Samples

Download data: TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing

Platform:

GPL11154

13 Samples

Download data: BW

(Submitter supplied) Purpose: The goals of this study are to compare the transcriptomic profile (mRNA-seq) of HD and control patient iPSC-derived neural cells to identify alterations in gene expression Methods: RNA were isolated from HD and control iPSC-derived neural cells. mRNAseq using Illumina Truseq mRNA PolyA+ v2 lib prep and Hiseq 2000. Statistical difference in mRNA levels were calculated with subsequent GO and pathway analysis Results: mRNAseq and statistical analysis revealed 1869 differentially expressed genes between HD and control iPSC-derived neural cells. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

7 Samples

Download data: TXT

(Submitter supplied) The goals of this study are to compare the epigenetic states of HD and control patient iPSC-derived neural cells to identify differences in chromatin state. We performed ChIP-seq in these cell lines for H3K4me3, H3K27ac, and H3K36me3 in these cell lines and found significant epigenetic differences between HD and control-derived cells.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

6 Samples

Download data: BW

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens; Mus musculus

Type:

Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing

Platforms:

GPL16791 GPL17021

44 Samples

Download data: TXT

(Submitter supplied) Progressive motor alterations and selective death of striatal medium spiny neurons (MSNs) are key pathological hallmarks of Huntington's disease (HD), a neurodegenerative condition caused by a CAG trinucleotide repeat expansion in the coding region of the huntingtin (HTT) gene. Most research has focused on the pathogenic effects of the resultant protein product(s); however, growing evidence indicates that expanded CAG repeats within mutant HTT mRNA and derived small CAG repeat RNAs (sCAG) participate in HD pathophysiology. more...

Organism:

Homo sapiens

Type:

Non-coding RNA profiling by high throughput sequencing

Platform:

GPL16791

6 Samples

Download data: TXT

(Submitter supplied) Progressive motor alterations and selective death of striatal medium spiny neurons (MSNs) are key pathological hallmarks of Huntington's disease (HD), a neurodegenerative condition caused by a CAG trinucleotide repeat expansion in the coding region of the huntingtin (HTT) gene. Most research has focused on the pathogenic effects of the resultant protein product(s); however, growing evidence indicates that expanded CAG repeats within mutant HTT mRNA and derived small CAG repeat RNAs (sCAG) participate in HD pathophysiology. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

38 Samples

Download data: TXT

(Submitter supplied) Protein kinase CK2 alpha prime (CK2a') is preferentially upregulated in the striatum of patients with HD and in different cellular and mouse models of HD. CK2a' happloinsufficiency in the zQ175 HD mouse model restored several HD-like phenotypes. We hypothesized that CK2a' neuronal up-regulation is linked to key transcriptional alterations in the zQ175 mouse model. We found that CK2a' haploinsufficiency rescued the expression of genes associated with synaptogenesis and glutamatergic signaling whose upstream regulator seems to be alpha-synuclein. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

18 Samples

Download data: TXT

(Submitter supplied) The polyglutamine expansion in huntingtin (Htt) protein is a cause of Huntington’s disease (HD). Htt is an essential gene as deletion of the mouse Htt gene homolog (Hdh) is embryonic lethal in mice. Therefore, in addition to elucidating the mechanisms responsible for polyQ-mediated pathology, it is also important to understand the normal function of Htt protein for both basic biology and for HD. To systematically search for a mouse Htt function, we took advantage of the Hdh +/- and Hdh-floxed mice and generated four mouse embryonic fibroblast (MEF) cells lines which contain a single copy of the Hdh gene (Hdh-HET) and four MEF lines in which the Hdh gene was deleted (Hdh-KO). more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6731

12 Samples

Download data: TXT

(Submitter supplied) Identification of transcriptional changes in Huntington's disease (HD) and normal (WT) human embryonic stem cells (hESC)- and induced pluripotent stem cells(iPSC)-derived striatal GABAergic neruons.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

42 Samples

Download data: TXT

(Submitter supplied) We used cell-specific zinc finger protein (ZFP) transcriptional repressors to lower mHTT and experimentally evaluated the consequences of neuronal and astrocytic mHTT lowering on HD pathophysiology using cell-type specific RNA-seq

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

62 Samples

Download data: XLSX

(Submitter supplied) We performed cell-type specific RNAseq in astrocytes and neurons in the presence or absence of ZFP transcriptional repressors in the striatum of R6/2 mouse model of HD.

Organism:

Mus musculus

Type:

Other

Platform:

GPL21103

110 Samples

Download data: TXT