Similar studies for GEO DataSets (Select 200064386) - GEO DataSets

Select item 2000643861.

N17 Modifies Mutant Huntingtin Nuclear Pathogenesis and Severity of Disease in HD BAC Transgenic Mice

(Submitter supplied) Longitudinal microarray data from BACHD-ΔN17 mice with wildtype littermate controls

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL6885
48 Samples

Download data: TXT

Series

Accession:: GSE64386

ID:: 200064386

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2001572872.

RNA-sequencing of Drosophila expressing mutant Huntingtin in neurons or glia

(Submitter supplied) We performed RNA-seq on head tissue collected from Drosophila expressing N-terminal (UAS-HTTNT231Q128) or full-length (UAS-HTTFL200Q) human mHTT in neurons (elav-GAL4) or glia (repo-GAL4).

Organism:: Drosophila melanogaster

Type:: Expression profiling by high throughput sequencing

Platform:: GPL17275
72 Samples

Download data: TXT

Series

Accession:: GSE157287

ID:: 200157287

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 2000102633.

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

Select item 2000102024.

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

Select item 2000098575.

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

Select item 2000098046.

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

Select item 2000098037.

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

Select item 2000093758.

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

Select item 2000079589.

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

Select item 20002523210.

In vivo cell-autonomous transcriptional abnormalities revealed in mice expressing mutant huntingtin in striatal but not cortical neurons

(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

Series

Accession:: GSE25232

ID:: 200025232

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20005444311.

Mutant Huntingtin promotes neuronal death through cell autonomous microglial activation via myeloid lineage- determining factors

(Submitter supplied) Huntington's Disease (HD) is a fatal neurodegenerative disorder caused by an extended polyglutamine repeat in the N-terminus of the huntingtin (Htt) protein. Reactive microglia and elevated cytokine levels are observed in the brains of HD patients, but the extent to which neuroinflammation results from extrinsic or cell-autonomous mechanisms is unknown. Furthermore, the impact of microglia activation on the pathogenesis of HD remains to be established. more...

Organism:: Mus musculus

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

Platforms:: GPL11002 GPL13112
22 Samples

Download data: BED, TXT

Series

Accession:: GSE54443

ID:: 200054443

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20013505712.

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

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20016669513.

Mutant huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease (mRNA-Seq)

(Submitter supplied) The polyglutamine expansion of huntingtin (mHtt) causes Huntington disease (HD) and neurodegeneration, but the mechanisms remain unclear. Here, we found that mHtt promotes ribosome stalling and suppresses protein synthesis. Depletion of mHtt enhances protein synthesis and increases the speed of ribosome translocation, while mHtt directly inhibits protein synthesis in vitro. We found interactions of ribosomal proteins and translating ribosomes with mHtt. more...

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL19057
4 Samples

Download data: XLSX

Series

Accession:: GSE166695

ID:: 200166695

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20014667514.

Mutant huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease.

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

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing; Other

Platform:: GPL19057
22 Samples

Download data

Series

Accession:: GSE146675

ID:: 200146675

PubMed Full text in PMC Similar studies

Select item 20014667415.

Mutant huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease [Ribo-seq]

(Submitter supplied) The polyglutamine expansion of huntingtin (mHtt) causes Huntington disease (HD) and neurodegeneration, but the mechanisms remain unclear. Here, we found that mHtt promotes ribosome stalling and suppresses protein synthesis. Depletion of mHtt enhances protein synthesis and increases the speed of ribosome translocation, while mHtt directly inhibits protein synthesis in vitro. We found interactions of ribosomal proteins and translating ribosomes with mHtt. more...

Organism:: Mus musculus

Type:: Other

Platform:: GPL19057
9 Samples

Download data: CSV

Series

Accession:: GSE146674

ID:: 200146674

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20014667316.

Mutant huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease [RNA-seq]

(Submitter supplied) The polyglutamine expansion of huntingtin (mHtt) causes Huntington disease (HD) and neurodegeneration, but the mechanisms remain unclear. Here, we found that mHtt promotes ribosome stalling and suppresses protein synthesis. Depletion of mHtt enhances protein synthesis and increases the speed of ribosome translocation, while mHtt directly inhibits protein synthesis in vitro. We found interactions of ribosomal proteins and translating ribosomes with mHtt. more...

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL19057
9 Samples

Download data: CSV

Series

Accession:: GSE146673

ID:: 200146673

PubMed Full text in PMC Similar studies SRA Run Selector

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