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Links from GEO DataSets

Items: 20

1.

Gene expression profiles of striatum and cerebellum from knock-in mouse model of Huntington's disease

(Submitter supplied) Huntington’s disease (HD) involves marked early neurodegeneration in the striatum whereas the cerebellum is relatively spared despite the ubiquitous expression of full-length mutant huntingtin, implying that inherent tissue-specific differences determine susceptibility to the HD CAG mutation. To understand this tissue specificity, we compared early mutant huntingtin-induced gene expression changes in striatum to those in cerebellum in young Hdh CAG knock-in mice, prior to onset of evident pathological alterations. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS3935
Platform:
GPL1261
24 Samples
Download data: CEL
Series
Accession:
GSE9038
ID:
200009038
2.
Full record GDS3935

Huntington's disease CAG knock-in effect on striatum and cerebellum

Analysis of striatum and cerebellum of HdhQ111/Q111 CAG knock-ins (expressing full-length huntingtin with 111-glutamines) and wild-type HdhQ7/Q7 mice (expressing full-length huntingtin with 7-glutamines). Results provide insight into tissue-specific differences in susceptibility to HD CAG mutation.
Organism:
Mus musculus
Type:
Expression profiling by array, transformed count, 2 genotype/variation, 2 tissue sets
Platform:
GPL1261
Series:
GSE9038
24 Samples
Download data: CEL
3.

Mutant huntingtin's effects on striatal gene expression in mice

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array
Platforms:
GPL81 GPL1261
32 Samples
Download data: CEL
Series
Accession:
GSE10263
ID:
200010263
4.

Striatal gene expression data from 22-month-old CHL2 mice and control mice.

(Submitter supplied) Achieving a mechanistic understanding of disease and initiating preclinical therapeutic trials necessitate the study of huntingtin toxicity and its remedy in model systems. To allow the engagement of appropriate experimental paradigms, Huntington’s disease (HD) models need to be validated in terms of how they recapitulate a particular aspect of human disease. In order to examine transcriptome-related effects of mutant huntingtin, we compared striatal mRNA profiles from seven genetic mouse models of disease to that of postmortem human HD caudate using microarray analysis. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
8 Samples
Download data: CEL
Series
Accession:
GSE10202
ID:
200010202
5.

Striatal gene expression data from 12 weeks-old R6/2 mice and control mice

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
18 Samples
Download data: CEL
Series
Accession:
GSE9857
ID:
200009857
6.

Striatal gene expression data from 12 weeks-old R6/2 mice and control mice (set 2)

(Submitter supplied) To test the hypotheses that mutant huntingtin protein length and wild-type huntingtin dosage have important effects on disease-related transcriptional dysfunction, we compared the changes in mRNA in seven genetic mouse models of Huntington's disease (HD) and postmortem human HD caudate. Transgenic models expressing short N-terminal fragments of mutant huntingtin (R6/1 and R6/2 mice) exhibited the most rapid effects on gene expression, consistent with previous studies. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
9 Samples
Download data: CEL
Series
Accession:
GSE9804
ID:
200009804
7.

Striatal gene expression data from 12 weeks-old R6/2 mice and control mice (set 1)

(Submitter supplied) To test the hypotheses that mutant huntingtin protein length and wild-type huntingtin dosage have important effects on disease-related transcriptional dysfunction, we compared the changes in mRNA in seven genetic mouse models of Huntington's disease (HD) and postmortem human HD caudate. Transgenic models expressing short N-terminal fragments of mutant huntingtin (R6/1 and R6/2 mice) exhibited the most rapid effects on gene expression, consistent with previous studies. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
9 Samples
Download data: CEL
Series
Accession:
GSE9803
ID:
200009803
8.

Striatal gene expression data from 12 months-old Hdh4/Q80 mice and control mice.

(Submitter supplied) To test the hypotheses that mutant huntingtin protein length and wild-type huntingtin dosage have important effects on disease-related transcriptional dysfunction, we compared the changes in mRNA in seven genetic mouse models of Huntington's disease (HD) and postmortem human HD caudate. Transgenic models expressing short N-terminal fragments of mutant huntingtin (R6/1 and R6/2 mice) exhibited the most rapid effects on gene expression, consistent with previous studies. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL81
6 Samples
Download data: CEL
Series
Accession:
GSE9375
ID:
200009375
9.

Striatal gene expression data from 3- and 18-month-old Q92 mice and control mice.

(Submitter supplied) Achieving a mechanistic understanding of disease and initiating preclinical therapeutic trials necessitate the study of huntingtin toxicity and its remedy in model systems. To allow the engagement of appropriate experimental paradigms, Huntington’s disease (HD) models need to be validated in terms of how they recapitulate a particular aspect of human disease. In order to examine transcriptome-related effects of mutant huntingtin, we compared striatal mRNA profiles from seven genetic mouse models of disease to that of postmortem human HD caudate using microarray analysis. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
12 Samples
Download data: CEL
Series
Accession:
GSE7958
ID:
200007958
10.

Transcriptional correlates of pathological phenotype in a Huntington’s disease mouse model

(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
Series
Accession:
GSE135057
ID:
200135057
11.

Dense time series gene expression data from striatum of Huntington’s disease CAG knock-in mice across multiple genetic backgrounds

(Submitter supplied) Huntington’s disease is a dominantly inherited neurodegenerative disease caused by the expansion of a CAG repeat in the HTT gene. In addition to the length of the CAG expansion, factors such as genetic background have been shown to contribute to the age at onset of neurological symptoms. A central challenge in understanding the disease progression that leads from the HD mutation to massive cell death in the striatum is the ability to characterize the subtle and early functional consequences of the CAG expansion longitudinally. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL10787
791 Samples
Download data: TXT
Series
Accession:
GSE88920
ID:
200088920
12.

Microarray gene expression data from Hdh knock-out, wild-type and knock-in embryonic stem cells

(Submitter supplied) Huntington's disease (HD) features a unique disease-initiating mechanism hypothesized to entail an impact of the CAG repeat encoded polyglutamine region on the full-length huntingtin protein, with dominant effects that are continuous with CAG size, in a simple gain of function. To evaluate these predictions, we generated a series of heterozygous Hdh CAG knock-in mouse embryonic stem (ES) cell lines, with 18, 48, 89, 109 CAGs, and found that a continuous analytic strategy efficiently identified, from genome-wide datasets, 73 genes and 172 pathways whose expression varied continuously with CAG length. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS4533
Platform:
GPL1261
24 Samples
Download data: CEL
Series
Accession:
GSE26001
ID:
200026001
13.
Full record GDS4533

Huntington's disease Hdh knock-out and knock-in embryonic stem cells

Analysis of embryonic stem cells without Hdh or with knock-in alleles with different Hdh CAG-polyglutamine repeat sizes. CAG-repeat length is inversely correlated with the age of onset of Huntington's disease (HD) symptoms in humans. Results provide insight into molecular mechanisms underlying HD.
Organism:
Mus musculus
Type:
Expression profiling by array, transformed count, 6 cell line, 3 genotype/variation, 7 other sets
Platform:
GPL1261
Series:
GSE26001
24 Samples
Download data: CEL
14.

Expression data from human Huntington fibroblasts

(Submitter supplied) Gene expression profile comparison from fibroblasts of Huntington individuals and normal ones We used microarrays to detail the global gene expression of fibroblasts from Huntington patients
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
9 Samples
Download data: CEL, CHP
Series
Accession:
GSE45516
ID:
200045516
15.

Genome-wide analysis of RARβ transcriptional targets in mouse striatum links retinoic acid signaling with Huntington’s disease and other neurodegenerative disorders

(Submitter supplied) The active vitamin A derivative retinoic acid (RA) is an important regulator of adult brain functions. How these regulations are achieved is poorly known, partly due to the paucity of information on RA molecular targets. The striatum, the region involved in control of motor, cognitive and affective functions, may be particularly prone to such regulation as it displays the highest levels of RA and its receptors (RARs). more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
3 Samples
Download data: TXT
Series
Accession:
GSE67829
ID:
200067829
16.

Genome-wide analysis of RARβ transcriptional targets in mouse striatum links retinoic acid signaling with Huntington’s disease and other neurodegenerative disorders

(Submitter supplied) Transcriptome analysis of nucleus accumbens shell samples from RARβ-null mutant mice and their wild type littermates The active vitamin A derivative retinoic acid (RA) is an important regulator of adult brain functions. How these regulations are achieved is poorly known, partly due to the paucity of information on RA molecular targets. The striatum, the region involved in control of motor, cognitive and affective functions, may be particularly prone to such regulation as it displays the highest levels of RA and its receptors (RARs). more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
11 Samples
Download data: CEL, CHP
Series
Accession:
GSE67761
ID:
200067761
17.

A novel approach to investigate tissue-specific trinucleotide repeat instability

(Submitter supplied) In Huntington’s disease (HD), an expanded CAG repeat produces characteristic striatal neurodegeneration. Interestingly, the HD CAG repeat, whose length determines age at onset, undergoes tissue-specific somatic instability, predominant in the striatum, suggesting that tissue-specific CAG length changes could modify the disease process. Therefore, understanding the mechanisms underlying the tissue specificity of somatic instability may provide novel routes to therapies. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS4534
Platform:
GPL1261
12 Samples
Download data: CEL
Series
Accession:
GSE19780
ID:
200019780
18.

A novel approach to investigate tissue-specific trinucleotide repeat instability - A validation set of prediction model

(Submitter supplied) In Huntington’s disease (HD), an expanded CAG repeat produces characteristic striatal neurodegeneration. Interestingly, the HD CAG repeat, whose length determines age at onset, undergoes tissue-specific somatic instability, predominant in the striatum, suggesting that tissue-specific CAG length changes could modify the disease process. Therefore, understanding the mechanisms underlying the tissue specificity of somatic instability may provide novel routes to therapies. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
2 Samples
Download data: CEL
Series
Accession:
GSE9025
ID:
200009025
19.
Full record GDS4534

HdhQ111 knock-in model of Huntington's disease: striatum and cerebellum

Analysis of striatum and cerebellum from a HdhQ111/111 knock-in model of Huntington's disease (HD). The 10-week HdhQ111/111 mice exhibit somatic instability in striatum but not in cerebellum. Results provide insight into the molecular basis of tissue-specific somatic instability.
Organism:
Mus musculus
Type:
Expression profiling by array, transformed count, 2 genotype/variation, 2 tissue sets
Platform:
GPL1261
Series:
GSE19780
12 Samples
Download data: CEL
20.

Transcriptome profiling in knock-in mouse models of Huntington's disease [Striatum_miRNA]

(Submitter supplied) Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder that is characterized by motor, cognitive, and psychiatric alterations. The mutation responsible for this disease is an abnormally expanded and unstable CAG repeat within the coding region of the gene encoding huntingtin (Htt). Knock-in mouse models of HD with human exon 1 containing expanded CAG repeats inserted in the murine huntingtin gene (Hdh) provide a genetic reconstruction of the human causative mutation within the mouse model. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
96 Samples
Download data: XLSX
Series
Accession:
GSE78793
ID:
200078793
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