U.S. flag

An official website of the United States government

Format
Items per page
Sort by

Send to:

Choose Destination

Links from GEO DataSets

Items: 16

1.

Longitudinal modeling of human neuronal aging reveals the contribution of the RCAN1-TFEB pathway to Huntington's disease neurodegeneration

(Submitter supplied) Aging is a common risk factor in neurodegenerative disorders and the ability to investigate aging of neurons in an isogenic background would facilitate discovering the interplay between neuronal aging and onset of neurodegeneration. Here, we perform direct neuronal reprogramming of longitudinally collected human fibroblasts to reveal genetic pathways altered at different ages. Comparative transcriptome analysis of longitudinally aged striatal medium spiny neurons (MSNs), a primary neuronal subtype affected in Huntington's disease (HD), identified pathways associated with RCAN1, a negative regulator of calcineurin. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
24 Samples
Download data: XLSX
Series
Accession:
GSE241430
ID:
200241430
2.

Mechanism for the modifier effect of RCAN1 in neurodegeneration of Huntington’s disease in patient-derived neurons [ATAC-Seq]

(Submitter supplied) Genome-wide association studies have identified Genetic Modifiers of HD (GeM-HD) comprised of polymorphic gene variants associated with accelerated or delayed onset of Huntington’s disease (HD). However, GeM-HD genes that contribute to neurodegeneration in HD remain underexplored. Here, we used medium spiny neurons (MSNs) directly reprogrammed from fibroblasts of symptomatic HD patients (HD-MSNs), which recapitulate adult-onset neurodegenerative pathology of HD, to uncover genes whose reduced function alleviated HD-associated neurodegeneration. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
36 Samples
Download data: BIGWIG
Series
Accession:
GSE210996
ID:
200210996
3.

Age- and stage-dependent degeneration of Huntington’s disease neurons is linked to declining autophagy mediated by mir-29b-3p

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
106 Samples
Download data: BIGWIG
Series
Accession:
GSE194243
ID:
200194243
4.

Age- and stage-dependent degeneration of Huntington’s disease neurons is linked to declining autophagy mediated by mir-29b-3p (Figure 5, 7 and S4)

(Submitter supplied) Direct neuronal conversion of fibroblasts from Huntington’s disease (HD) patients to striatal medium spiny neurons (MSNs) has been shown to recapitulate neurodegenerative pathology of HD. Here, we carried out comparative analyses between reprogrammed MSNs from patients at different disease stages to investigate age-associated molecular processes driving neurodegeneration. We found that neuronal death was manifested in reprogrammed MSNs from symptomatic HD patients (HD-MSNs) compared to MSNs derived from younger, pre-symptomatic patients (pre-HD-MSNs) and healthy controls. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
34 Samples
Download data: BIGWIG
Series
Accession:
GSE194242
ID:
200194242
5.

Age-related Huntington's disease progression modeled in directly reprogrammed patient-derived striatal neurons highlights impaired autophagy (Figure 2 and S2)

(Submitter supplied) Direct neuronal conversion of fibroblasts from Huntington’s disease (HD) patients to striatal medium spiny neurons (MSNs) has been shown to recapitulate neurodegenerative pathology of HD. Here, we carried out comparative analyses between reprogrammed MSNs from patients at different disease stages to investigate age-associated molecular processes driving neurodegeneration. We found that neuronal death was manifested in reprogrammed MSNs from symptomatic HD patients (HD-MSNs) compared to MSNs derived from younger, pre-symptomatic patients (pre-HD-MSNs) and healthy controls. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
72 Samples
Download data: XLSX
Series
Accession:
GSE194241
ID:
200194241
6.

Striatal genes regulated by super-enhancers and displaying low paused RNAPII are preferentially down-regulated in Huntington's disease

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL13112
15 Samples
Download data: BEDGRAPH, WIG
Series
Accession:
GSE59572
ID:
200059572
7.

Striatal genes regulated by super-enhancers and displaying low paused RNAPII are preferentially down-regulated in Huntington’s disease [RNA-seq]

(Submitter supplied) Huntington neurodegenerative disease (HD) is associated with extensive down-regulation of neuronal genes. We show preferential down-regulation of super-enhancer-regulated neuronal function genes in the striatum of HD mice. Striatal super-enhancers display extensive H3K27 acetylation within gene bodies and drive transcription characterized by low levels of paused RNAPII. Down-regulation of gene expression is associated with diminished H3K27 acetylation and RNAPII recruitment. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
5 Samples
Download data: BEDGRAPH, XLSX
Series
Accession:
GSE59571
ID:
200059571
8.

Striatal genes regulated by super-enhancers and displaying low paused RNAPII are preferentially down-regulated in Huntington’s disease [ChIP-seq]

(Submitter supplied) Huntington neurodegenerative disease (HD) is associated with extensive down-regulation of neuronal genes. We show preferential down-regulation of super-enhancer-regulated neuronal function genes in the striatum of HD mice. Striatal super-enhancers display extensive H3K27 acetylation within gene bodies and drive transcription characterized by low levels of paused RNAPII. Down-regulation of gene expression is associated with diminished H3K27 acetylation and RNAPII recruitment. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
10 Samples
Download data: WIG
Series
Accession:
GSE59570
ID:
200059570
9.

The transcriptional response to PPP3R1

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL8321
12 Samples
Download data: CEL
Series
Accession:
GSE56673
ID:
200056673
10.

Expression data from PPP3R1 cell line starved as compared to PPP3R1 cell line grown in Normal Medium

(Submitter supplied) In order to identify the effects of starvation on the PPP3R1 cell line trascriptome, we performed Affymetrix Gene-Chip hybridization experiments for the starved cells Transcriptome analysis of the starved PPP3R1 cell line
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL8321
6 Samples
Download data: CEL
Series
Accession:
GSE56672
ID:
200056672
11.

Expression data from MEFs wt cells starved as compared to MEFs wt cells grown in Normal Medium

(Submitter supplied) In order to identify the effects of starvation on the MEFs wt trascriptome, we performed Affymetrix Gene-Chip hybridization experiments for the starved cells Transcriptome analysis of the starved MEFs wt cells
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL8321
6 Samples
Download data: CEL
Series
Accession:
GSE56671
ID:
200056671
12.

Gene expression profile in stable RCAN1-4 knockdown thyroid cancer cell lines

(Submitter supplied) To explore the effects of endogenous RCAN1-4 loss on thyroid cancer in vivo, we developed RCAN1-4 knockdown stable cells. Subcutaneous xenograft models demonstrated that RCAN1-4 knockdown promotes tumor growth. Intravenous metastasis models demonstrated that RCAN1-4 loss promotes tumor metastases to the lungs and their subsequent growth. Microarray was performed to understand how RCAN1-4 regulates tumor behaviors and the global effects of RCAN1-4 knockdown in these cells.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17586
12 Samples
Download data: CEL, CHP
Series
Accession:
GSE93250
ID:
200093250
13.

Identification of MCIP1 as an ATF6-inducible ER Stress Response Gene in the Heart by Gene Expression Profiling

(Submitter supplied) We recently found that the endoplasmic reticulum (ER) stress response (ERSR) is activated in surviving cardiac myocytes in a mouse model of in vivo myocardial infarction. ATF6 is an ER stress-activated transcription factor that induces ERSR genes, some of which encode proteins that may protect against ischemic damage. However, few ERSR genes have been identified in the heart, and there have been no gene expression profiling studies of ATF6-inducible genes, in vivo. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS3667
Platform:
GPL1261
12 Samples
Download data: CEL, CHP
Series
Accession:
GSE8322
ID:
200008322
14.
Full record GDS3667

Transgenic model of selective ATF6 activation: heart

Analysis of heart left ventricle from ATF6-MER transgenic (TG) males, treated with tamoxifen to confer activation to ATF6-MER. Activating ATF6 protects the heart of TG animals from endoplasmic reticulum stress. Results provide insight into molecular mechanisms underlying this protective effect.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 agent, 2 genotype/variation sets
Platform:
GPL1261
Series:
GSE8322
12 Samples
Download data: CEL, CHP
15.

Analysis of differentially expressed genes between Huntington’s disease and control iPSCs derived GABA MS-like neurons

(Submitter supplied) Huntington’s disease (HD) is an incurable hereditary neurodegenerative disorder, which manifests itself as a loss of GABAergic medium spiny (GABA MS) neurons in the striatum and caused by an expansion of the CAG repeat in exon 1 of the huntingtin gene. There is no cure for HD, existing pharmaceutical can only relieve its symptoms. Here, induced pluripotent stem cells were established from patients with low CAG repeat expansion in the huntingtin gene, and were then efficiently differentiated into GABA MS-like neurons under defined culture conditions. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
12 Samples
Download data: TXT
Series
Accession:
GSE77558
ID:
200077558
16.

Study of the effect of Protein Kinase CK2 alpha prime in the transcriptional deficits associated with Huntington's disease

(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
Series
Accession:
GSE160586
ID:
200160586
Format
Items per page
Sort by

Send to:

Choose Destination

Supplemental Content

db=gds|term=|query=1|qty=3|blobid=MCID_674d8e93629932298a515ca4|ismultiple=true|min_list=5|max_list=20|def_tree=20|def_list=|def_view=|url=/Taxonomy/backend/subset.cgi?|trace_url=/stat?
   Taxonomic Groups  [List]
Tree placeholder
    Top Organisms  [Tree]

Find related data

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Support Center