GEO DataSets

(Submitter supplied) The molecular mechanisms that lead to the cognitive defects characteristic of Down syndrome (DS), the most frequent cause of mental retardation, have remained elusive. Here we use a transgenic DS mouse model to show that DYRK1A gene dosage imbalance deregulates chromosomal clusters of genes located near neuron-restrictive silencer factor (REST/NRSF) binding sites. We found that DYRK1A binds the SWI/SNF-complex known to interact with REST/NRSF. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL2872

4 Samples

Download data: GPR

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

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL2872

9 Samples

Download data: GPR

(Submitter supplied) Transcription profiling of transgenic down syndrome mouse model to show the role of DYRK1A gene. The molecular mechanisms that lead to the cognitive defects characteristic of Down syndrome (DS), the most frequent cause of mental retardation, have remained elusive. Here we use a transgenic DS mouse model to show that DYRK1A gene dosage imbalance deregulates chromosomal clusters of genes located near neuron-restrictive silencer factor (REST/NRSF) binding sites. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL7877

5 Samples

Download data: GPR

(Submitter supplied) The molecular mechanisms that lead to the cognitive defects characteristic of Down syndrome (DS), the most frequent cause of mental retardation, have remained elusive. Here we use a transgenic DS mouse model to show that DYRK1A gene dosage imbalance deregulates chromosomal clusters of genes located near neuron-restrictive silencer factor (REST/NRSF) binding sites. We found that DYRK1A binds the SWI/SNF-complex known to interact with REST/NRSF. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL2872

5 Samples

Download data: GPR

(Submitter supplied) The vertebrate-specific transcription factor RE-1 silencing transcription factor or neuron-restrictive silencer factor (REST/NRSF) was first described as a negative regulator restricting expression of neuronal genes to neurons in a variety of genetic contexts. However, REST/NRSF has a more general role in the regulation of gene expression that involves chromatin remodelling via a SWI/SNF complex. We identified a 677 gene repertoire of potential REST/NRSF-dependent genes taking advantage of Rest/Nrsf gene silencing in a mouse cell line. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL2872

6 Samples

Download data: GPR

(Submitter supplied) Using Illumina 450K arrays, 1.85% of analyzed CpG sites were hypermethylated and 0.31% hypomethylated in fetal Down syndrome (DS) cortex throughout the genome. The vast majority of differentially methylated promoters and genes was hypermethylated in DS and located outside chromosome 21, including the γ-protocadherin (PCDHG) cluster on chromosome 5q31, which is crucial for neural circuit formation in the developing brain. more...

Organism:

Homo sapiens

Type:

Methylation profiling by array

Platform:

GPL13534

72 Samples

Download data: TXT

(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

41 Samples

Download data: WIG

(Submitter supplied) Genes encoding subunits of SWI/SNF (BAF) chromatin remodeling complexes are collectively altered in over 20% of all human malignancies, but the mechanisms by which these complexes alter chromatin to modulate transcription and control cell fate are poorly understood. Utilizing both loss-of-function and gain-of-function approaches, here we show that SWI/SNF complexes are preferentially targeted to distal enhancers and interact with p300 to regulate transcription via modulation of histone H3 lysine 27 acetylation. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

6 Samples

Download data: WIG

(Submitter supplied) Genes encoding subunits of SWI/SNF (BAF) chromatin remodeling complexes are collectively altered in over 20% of all human malignancies, but the mechanisms by which these complexes alter chromatin to modulate transcription and control cell fate are poorly understood. Utilizing both loss-of-function and gain-of-function approaches, here we show that SWI/SNF complexes are preferentially targeted to distal enhancers and interact with p300 to regulate transcription via modulation of histone H3 lysine 27 acetylation. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL13112

35 Samples

Download data: BED, WIG

(Submitter supplied) Repressor element-1 silencing transcription factor (REST) or neuron-restrictive silencer factor (NRSF) is a zinc-finger (ZF) containing transcriptional repressor that recognizes thousands of neuron-restrictive silencer elements (NRSEs) in mammalian genomes. How REST/NRSF regulates gene expression remains incompletely understood. Here, we investigate the binding pattern and regulation mechanism of REST/NRSF in the clustered protocadherin (PCDH) genes. more...

Organism:

Homo sapiens; Mus musculus

Type:

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

4 related Platforms

95 Samples

Download data: BEDGRAPH, TXT, XLS

(Submitter supplied) We reported loss of ARID1A promoted neurogenesis and inhibited cardiogenesis. Here we used specific ARID1A antibody to pull down ARID1A binding genomic DNA in human embryonic stem cells, which let us know the potential genes regulated by ARID1A during neurogenesis and inhibited cardiogenesis. IgG was used as the control.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL18573 GPL20301

2 Samples

Download data: BW, NARROWPEAK

(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

Platforms:

GPL24676 GPL18573

8 Samples

Download data: BW, NARROWPEAK, TAR

(Submitter supplied) We reported loss of ARID1A promoted neurogenesis and inhibited cardiogenesis. Under microscopy, we observed that spontaneously differentiated cells were induced in ARID1A KO H9 hESCs cultured in mTesR medium. After cardiac differentiation for 10 days, we also observed the cell types were totally different between WT and ARID1A KO cells. We did not know what cells types were. Here scRNA-seq were used to identify the cell types in WT H9 hESCs and ARID1A KO H9 hESCs.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL24676 GPL18573

4 Samples

Download data: TAR

(Submitter supplied) We reported loss of ARID1A promoted neurogenesis and inhibited cardiogenesis. Under microscopy, we observed that spontaneously differentiated cells were induced in ARID1A KO H9 hESCs cultured in mTesR medium. We did not know what cells types were. Here ATAC-seq were used to investigate chromatin accessibilities change in differentiated (day 4) WT H9 hESCs and ARID1A KO hESC cells.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL24676

2 Samples

Download data: BW

(Submitter supplied) We reported loss of ARID1A promoted neurogenesis and inhibited cardiogenesis. Here we used specific ARID1A antibody to pull down ARID1A binding genomic DNA in human embryonic stem cells, which let us know the potential genes regulated by ARID1A during neurogenesis and inhibited cardiogenesis. 1% Input sample was collected from the same sample after chromatin shearing.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL18573

2 Samples

Download data: BW, NARROWPEAK

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

Organism:

Mus musculus; Homo sapiens

Type:

Expression profiling by high throughput sequencing

4 related Platforms

75 Samples

Download data: RESULTS, TAR

(Submitter supplied) Early-life adversity (ELA) is associated with lifelong memory deficits, yet the responsible mechanisms remain unclear. We imposed ELA by rearing rat pups in simulated poverty, assessed hippocampal memory, and probed changes in gene expression, their transcriptional regulation and the consequent changes in hippocampal neuronal structure. ELA rats had poor hippocampal memory and stunted hippocampal pyramidal neurons, associated with ~140 differentially expressed genes. more...

Organism:

Rattus norvegicus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18694

9 Samples

Download data: TXT