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Links from GEO DataSets

Items: 20

1.
Full record GDS2391

PGC-1alpha transcriptional coactivator null mutation effect on the brain striatum

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
Download data
DataSet
Accession:
GDS2391
ID:
2391
2.

Gene Expression Profiling of PGC-1a KO mouse striata

(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
Download data
Series
Accession:
GSE5786
ID:
200005786
3.

Huntington's disease: Gene expression changes caused by Hdh CAG mutation or 3-nitropropionic acid in striatal cells

(Submitter supplied) Affymetrix MG430 2.0 expression levels of wild-type (STHdhQ7/Q7), 3NP-treated wild-type (STHdhQ7/Q7+3-NP), and mutant (STHdhQ111/Q111) striatal cells Keywords: Pharmacological and genetic HD cell culture models
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS2911
Platform:
GPL1261
9 Samples
Download data: CEL
Series
Accession:
GSE3583
ID:
200003583
4.
Full record GDS2911

Huntington's disease models

Comparison of striatal cells harboring a mutant huntingtin protein with 111 glutamines to wild type striatal cells treated with 3-nitropropionic acid (3-NP). The size of the polyglutamine tract in huntingtin is correlated with mitochondrial function. 3-NP is a respiratory chain inhibitor.
Organism:
Mus musculus
Type:
Expression profiling by array, transformed count, 2 agent, 2 genotype/variation sets
Platform:
GPL1261
Series:
GSE3583
9 Samples
Download data: CEL
5.

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
6.

Next Generation Sequencing Investigation of altered transcripts in presence of dominant-negative transcription factor

(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
Series
Accession:
GSE74583
ID:
200074583
7.

lipin 1beta overexpression in mouse liver

(Submitter supplied) Mutations in the gene encoding lipin 1 cause hepatic steatosis in fld mice, a genetic model of lipodystrophy. Lipin 1 appears to be highly involved in the control of fatty acid metabolism. Lipin 1 is most often located in the nucleus, but other studies suggest that lipin also has effects in the cytoplasm. However, the molecular function of lipin 1 is unclear. To evaluate the effects of activation of the lipin 1 system in liver, lipin 1beta was overexpressed in mouse liver using an adenoviral vector. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS2291
Platform:
GPL339
4 Samples
Download data
Series
Accession:
GSE5538
ID:
200005538
8.
Full record GDS2291

Lipin 1-beta overexpression effect on the liver

Analysis of livers of transgenics overexpressing lipin 1-beta, an alternative form of lipin 1 containing a 33 amino acid insertion. Mutations in the gene encoding lipin 1 cause hepatic steatosis in fld animals, a genetic model of lipodystrophy. Results provide insight into the function of lipin 1.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 genotype/variation sets
Platform:
GPL339
Series:
GSE5538
4 Samples
Download data
DataSet
Accession:
GDS2291
ID:
2291
9.

mTOR pathway controls mitochondrial gene expression and respiration through the YY1/PGC-1alpha transcriptional complex

(Submitter supplied) Mitochondrial oxidative function is tightly controlled to maintain energy homeostasis in response to nutrient and hormonal signals. An important cellular component in the energy sensing response is the target of rapamycin (TOR) kinase pathway; however whether and how mTOR controls mitochondrial oxidative activity is unknown. Here, we show that mTOR kinase activity stimulates mitochondrial gene expression and oxidative function. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
12 Samples
Download data: CEL
Series
Accession:
GSE5332
ID:
200005332
10.

Complementary action of the PGC-1 coactivators in mitochondrial biogenesis and brown fat differentiation

(Submitter supplied) Mitochondria play an essential role in the ability of brown fat to generate heat, and the PGC-1 coactivators control several aspects of mitochondrial biogenesis. To investigate their specific roles in brown fat cells, we generated immortal preadipocyte lines from the brown adipose tissue of mice lacking PGC-1α. We could then efficiently knockdown PGC-1β expression by shRNA expression. Loss of PGC-1α did not alter brown fat differentiation but severely reduced the induction of thermogenic genes. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS2123
Platform:
GPL1261
6 Samples
Download data
Series
Accession:
GSE5042
ID:
200005042
11.

Expression of the brown fat thermogenic gene program requires PGC-1alpha

(Submitter supplied) To investigate the specific role of PGC-1 coactivators in brown fat cells, we generated immortal preadipocyte lines from the brown adipose tissue of mice lacking PGC-1alpha. We could then efficiently knockdown PGC-1beta expression by shRNA expression. Loss of PGC-1alpha did not alter brown fat differentiation but severly reduced the induction of thermogenic genes. In order to assess the specific requirement for PGC-1α in the global transcriptional response to cAMP, we used Affymetrix arrays to compare the sets of genes induced in response to a 4 hr dbcAMP treatment in differentiated wt and KO cells. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS2149
Platform:
GPL1261
8 Samples
Download data
Series
Accession:
GSE5041
ID:
200005041
12.
Full record GDS2149

PGC-1alpha null brown adipocyte response to cAMP

Analysis of PGC-1alpha null brown adipocytes treated with cAMP for 4 hours. PGC-1alpha is required for the thermogenic function of brown fat cells, and cAMP plays a role in thermogenesis. Results provide insight into the role of PGC-1alpha in the global transcriptional response to cAMP.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 agent, 2 genotype/variation sets
Platform:
GPL1261
Series:
GSE5041
8 Samples
Download data
DataSet
Accession:
GDS2149
ID:
2149
13.
Full record GDS2123

Brown fat cell response to PGC-1alpha and PGC-1beta deficiency

Analysis of brown fat cells lacking PGC-1alpha or both PGC-1alpha and PGC-1beta. PGC-1alpha is required for the thermogenic function of brown fat cells, and PGC-1beta is the closest homolog of PGC-1alpha. Results provide insight into the specific roles of PGC-1alpha and PGC-1beta in brown fat cells.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 3 agent, 2 genotype/variation sets
Platform:
GPL1261
Series:
GSE5042
6 Samples
Download data
DataSet
Accession:
GDS2123
ID:
2123
14.

Pyruvate induces mitochondrial biogenesis by a PGC-1alpha independent mechanism

(Submitter supplied) The present study examines the impact of altering energy provision on mitochondrial biogenesis in muscle cells. C2C12 myoblasts were chronically treated with supraphysiological levels of sodium pyruvate for 72 hr. Treated cells exhibited increased mitochondrial protein expression, basal respiratory rate and maximal oxidative capacity. The increase in mitochondrial biogenesis was independent of increases in PGC-1alpha and PGC-1alpha mRNA expression. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS2265
Platform:
GPL1261
6 Samples
Download data
Series
Accession:
GSE5497
ID:
200005497
15.
Full record GDS2265

Pyruvate effect on muscle cells

Analysis of C2C12 myoblasts treated with supraphysiological levels of sodium pyruvate for 72 hours. Pyruvate increases mitochondrial biogenesis in muscle myoblasts. Results provide insight into the impact of altering energy provision on mitochondrial biogenesis in muscle cells.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 agent sets
Platform:
GPL1261
Series:
GSE5497
6 Samples
Download data
DataSet
Accession:
GDS2265
ID:
2265
16.

The striatal kinase DCLK3 produces neuroprotection against mutant huntingtin

(Submitter supplied) The neurobiological functions of a number of kinases expressed in the brain are unknown. Here, we report new findings on DCLK3 (Doublecortin-like kinase 3) which is preferentially expressed in neurons in the striatum and dentate gyrus. Its function has never been investigated. DCLK3 expression is markedly reduced in Huntington's disease. Recent data obtained in studies related to cancer suggest DCLK3 could have anti-apoptotic effect. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17303
12 Samples
Download data: TXT
17.

Dysregulation of REST-regulated coding and non-coding RNAs in a cellular model of Huntington’s disease

(Submitter supplied) Abstract - Huntingtin (Htt) protein interacts with many transcriptional regulators, with widespread disruption to the transcriptome in Huntington’s disease (HD) brought about by altered interactions with the mutant Htt (muHtt) protein. Repressor Element-1 Silencing Transcription Factor (REST) is a repressor whose association with Htt in the cytoplasm is disrupted in HD, leading to increased nuclear REST and concomitant repression of several neuronal-specific genes, including brain-derived neurotrophic factor (Bdnf). more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6105
12 Samples
Download data: TXT
Series
Accession:
GSE42107
ID:
200042107
18.

ChIPSeq data from melanoma cancer cell line CHL-1 after Bromodomain and extra terminal (Bet) domain inhibitor treatment

(Submitter supplied) Bromodomain and extra terminal domain (BET) inhibition reduces occupancy of BET-family proteins at promoter and enhancer sites finally leading to genome wide changes in gene transcription. We used ChIPSeq profiling to investigate genome wide changes in promoter and enhancer occupancy induced by BET inhibitors BAY 1238097 and OTX-015, respectively.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
18 Samples
Download data: BW
Series
Accession:
GSE95585
ID:
200095585
19.

HDAC4 reduction: a novel therapeutic strategy to target cytoplasmic huntingtin and ameliorate neurodegeneration

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
71 Samples
Download data: CEL
Series
Accession:
GSE38237
ID:
200038237
20.

Gene expression data from cortex of 15w old WT, R6/2, HDAC4het and R6/2::HDAC4het mice

(Submitter supplied) Histone deacetylase (HDAC) 4 is a transcriptional repressor that contains a glutamine rich domain. We hypothesised that it may be involved in the molecular pathogenesis of Huntington’s disease (HD), a protein folding neurodegenerative disorder caused by an aggregation-prone polyglutamine expansion and transcriptional dysregulation. We found that HDAC4 interacts with huntingtin in a polyglutamine-length dependent manner and co-localises with cytoplasmic inclusions. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
34 Samples
Download data: CEL
Series
Accession:
GSE38219
ID:
200038219
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