GEO DataSets

(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) 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) 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 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) 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:

GPL20301 GPL18573

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:

GPL18573 GPL24676

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:

GPL18573 GPL24676

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) Embryos from the Dp1Tyb mouse model for Down syndrome (DS) present with congenital heart defects similar to the heart defects seen in humans with DS. We found that genetically reducing the copy number of the Dyrk1a gene (one of the genes in 3 copies in DS) from 3 to 2, normalised some of the transcriptomic changes in Dp1Tyb embryonic hearts and rescued congenital heart defects. Here we treated pregnant mice carrying Dp1Tyb and wild-type (WT) embryos with a Dyrk1a pharmacological inhibitor (Leucettinib-21 or L21) or an inactive isomer (Iso-L21) to study the effect of L21 on the transcriptome of Dp1Tyb and WT embryonic hearts.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

20 Samples

Download data: RESULTS

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

Organism:

Homo sapiens; Mus musculus

Type:

Expression profiling by high throughput sequencing

4 related Platforms

75 Samples

Download data: RESULTS, TAR

(Submitter supplied) We performed single cell RNAseq on whole hearts from E13.5 Dp1Tyb embryos and from wild-type littermates, as well as hearts from E13.5 Dp1TybDyrk1a+/+/- embryos and wild-type littermates. We identified 14 clusters which were assigned to individual cell types based on expression of marker genes.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

5 Samples

Download data: TAR

(Submitter supplied) We performed bulk RNAseq on whole hearts from E13.5 Dp1Tyb embryos and from wild-type littermates, as well as hearts from E13.5 Dp1TybDyrk1a+/+/- embryos and wild-type littermates. Analysis showed the expected increased expression of the Hsa21-orthologous genes on Mmu16 that are present in 3 copies. Gene set enrichment analysis identified pathways that are altered in Dp1Tyb hearts. Some of these changes were dependent on 3 copies of Dyrk1a.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

20 Samples

Download data: TXT

(Submitter supplied) We performed bulk RNAseq on whole hearts from E13.5 Dp3Tyb embryos and from wild-type littermates, as well as hearts from E13.5 Ts1Rhr embryos and wild-type littermates. Analysis showed the expected increased expression of the Hsa21-orthologous genes on Mmu16 that are present in 3 copies. Gene set enrichment analysis identified pathways that are altered in Dp3Tyb and Ts1Rhr hearts.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

20 Samples

Download data: TXT