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Links from GEO DataSets

Items: 20

1.

ChIP-Seq of Myf5, MyoD, Snai1, HDAC1, HDAC2, E47 and empty vector controls in mouse skeletal myoblasts or myotubes

(Submitter supplied) In skeletal myogenesis, the transcription factor MyoD activates distinct transcriptional programs in progenitors compared to terminally differentiated cells. Using ChIP-seq and gene expression analyses, we show that in primary myoblasts, Snail-HDAC1/2 repressive complex bind and exclude MyoD from its targets. Notably, Snail binds E-box motifs that are G/C-rich in their central dinucleotides, and such sites are almost exclusively associated with genes expressed during differentiation. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL9250 GPL11002
14 Samples
Download data: BW, TXT
Series
Accession:
GSE24852
ID:
200024852
2.

RNA-seq data of si-Snai1, si-Snai2, si-Snai1/2 and si-Scrambled treated mouse primary myoblasts

(Submitter supplied) In skeletal myogenesis, the transcription factor MyoD, activates distinct transcriptional programs in progenitors compared to terminally differentiated cells. Using ChIP-seq and gene expression analyses, we show that in primary myoblasts, Snai1/2-HDAC1/2 repressive complex bind and exclude MyoD from its targets. Notably, Snail binds E-box motifs that are G/C-rich in their central dinucleotides, and such sites are almost exclusively associated with genes expressed during differentiation. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11002
4 Samples
Download data: TXT
Series
Accession:
GSE38236
ID:
200038236
3.

Snail regulates MyoD binding-site occupancy to direct enhancer switching and differentiation-specific transcription in myogenesis

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11002 GPL9250 GPL6246
27 Samples
Download data: BW, CEL, TXT
Series
Accession:
GSE24904
ID:
200024904
4.

Time Series of gene expression during the course of myogenic differentiation in mouse skeletal muscle cells

(Submitter supplied) In skeletal myogenesis, the transcription factor MyoD activates distinct transcriptional programs in progenitors compared to terminally differentiated cells. Using ChIP-seq and gene expression analyses, we show that in primary myoblasts, Snail-HDAC1/2 repressive complex bind and exclude MyoD from its targets. Notably, Snail binds E-box motifs that are G/C-rich in their central dinucleotides, and such sites are almost exclusively associated with genes expressed during differentiation. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
9 Samples
Download data: CEL
Series
Accession:
GSE24811
ID:
200024811
5.

MUNC downregulation decreases muscle differentiation

(Submitter supplied) Gene expression profiling in differentiating C2C12 cells comparing control cells and MUNC-deprived cells
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6096
4 Samples
Download data: CEL
Series
Accession:
GSE63673
ID:
200063673
6.

MyoD and FoxO3 mediated hotspot interaction orchestrates super-enhancer activity during myogenic differentiation (Foxo3 ChIP-seq)

(Submitter supplied) Super-enhancers (SEs) are cis-regulatory elements enriching lineage specific key transcription factors (TFs) to form hotspots. A paucity of identification and functional dissection promoted us to investigate SEs during myoblast differentiation. ChIP-seq analysis of histone marks leads to the uncovering of SEs which remodel progressively during the course of differentiation. Further analyses of TF ChIP-seq enable the definition of SE hotspots co-bound by the master TF, MyoD and other TFs, among which we perform in-depth dissection for MyoD/FoxO3 interaction in driving the hotspots formation and SE activation.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11002
2 Samples
Download data: BED
Series
Accession:
GSE99207
ID:
200099207
7.

MyoD and FoxO3 mediated hotspot interaction orchestrates super-enhancer activity during myogenic differentiation

(Submitter supplied) Super-enhancers (SEs) are cis-regulatory elements enriching lineage specific key transcription factors (TFs) to form hotspots. A paucity of identification and functional dissection promoted us to investigate SEs during myoblast differentiation. ChIP-seq analysis of histone marks leads to the uncovering of SEs which remodel progressively during the course of differentiation. Further analyses of TF ChIP-seq enable the definition of SE hotspots co-bound by the master TF, MyoD and other TFs, among which we perform in-depth dissection for MyoD/FoxO3 interaction in driving the hotspots formation and SE activation.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18480 GPL19057
13 Samples
Download data: BED
Series
Accession:
GSE93916
ID:
200093916
8.

A KAP1 phosphorylation switch controls MyoD function during skeletal muscle differentiation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
9 Samples
Download data: BED, TXT
Series
Accession:
GSE62664
ID:
200062664
9.

A KAP1 phosphorylation switch controls MyoD function during skeletal muscle differentiation (ChIP-seq)

(Submitter supplied) The transcriptional activator MyoD serves as a master controller of myogenesis. Often in partnership with Mef2, MyoD binds to the promoters of hundreds of muscle genes in proliferating myoblasts, yet activates these targets only upon receiving cues that launch differentiation. What regulates this off/on switch of MyoD function has been incompletely understood, although known to reflect the action of chromatin modifiers. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
3 Samples
Download data: BED
Series
Accession:
GSE62660
ID:
200062660
10.

A KAP1 phosphorylation switch controls MyoD function during skeletal muscle differentiation (RNA-seq)

(Submitter supplied) The transcriptional activator MyoD serves as a master controller of myogenesis. Often in partnership with Mef2, MyoD binds to the promoters of hundreds of muscle genes in proliferating myoblasts, yet activates these targets only upon receiving cues that launch differentiation. What regulates this off/on switch of MyoD function has been incompletely understood, although known to reflect the action of chromatin modifiers. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: TXT
Series
Accession:
GSE62659
ID:
200062659
11.

Conversion of MyoD to a neurogenic factor: binding site specificity determines lineage

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
20 Samples
Download data
Series
Accession:
GSE64627
ID:
200064627
12.

Conversion of MyoD to a neurogenic factor: binding site specificity determines lineage [ChIP-seq]

(Submitter supplied) MyoD and NeuroD2 are master regulators of myogenesis and neurogenesis and bind to a "shared" E-box sequence (CAGCTG) and a "private" sequence (CAGGTG or CAGATG, respectively). To determine whether private-site recognition is sufficient to confer lineage-specification, we generated a MyoD-mutant with the DNA binding specificity of NeuroD2. Our results demonstrate that redirecting MyoD binding from MyoD-private sites to NeuroD2-private sites, despite preserved binding to the MyoD/NeuroD2-shared sites, is sufficient to change MyoD from a master regulator of myogenesis to a master regulator of neurogenesis.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
12 Samples
Download data: BED
Series
Accession:
GSE64626
ID:
200064626
13.

Conversion of MyoD to a neurogenic factor: binding site specificity determines lineage [RNA-seq]

(Submitter supplied) MyoD and NeuroD2 are master regulators of myogenesis and neurogenesis and bind to a "shared" E-box sequence (CAGCTG) and a "private" sequence (CAGGTG or CAGATG, respectively). To determine whether private-site recognition is sufficient to confer lineage-specification, we generated a MyoD-mutant with the DNA binding specificity of NeuroD2. Our results demonstrate that redirecting MyoD binding from MyoD-private sites to NeuroD2-private sites, despite preserved binding to the MyoD/NeuroD2-shared sites, is sufficient to change MyoD from a master regulator of myogenesis to a master regulator of neurogenesis.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: TXT
Series
Accession:
GSE64622
ID:
200064622
14.

Motif Variation Regulates the Affinity Landscape and Epigenetic State of the MyoD Cistrome

(Submitter supplied) The cis-regulatory code is the cellular lexicon by which the transcriptional machinery converts sequence information within cis-regulatory modules (CRMs) into gene expression output. Tissue-specific transcription factors such as MyoD orchestrate gene expression programs by binding to short DNA motifs called E-boxes within their target CRMs to modulate chromatin state and to fine-tune gene expression output. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11002
7 Samples
Download data: TXT, XLS
Series
Accession:
GSE80588
ID:
200080588
15.

Liaison between SNAI2 and MYOD enhances oncogenesis and suppresses differentiation in Fusion-Negative Rhabdomyosarcoma

(Submitter supplied) Rhabdomyosarcoma (RMS) is a pediatric malignancy of mesenchymal origin. Fusion Negative-RMS (FN-RMS) tumors are associated with RAS-pathway activation. RMS tumors express pro-differentiation myogenic transcription factors MYOD and MYOG, yet why they are unable to differentiate is poorly understood. Here we show that SNAI2 is highly expressed in FN-RMS, is regulated by MYOD and blocks myogenic differentiation promoting growth. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Other
Platform:
GPL18573
22 Samples
Download data: HIC, NARROWPEAK, TXT
16.

Knockdown of Ino80 complex subunits Actr5, Ies6, and Ino80 in RD cells

(Submitter supplied) INO80 complex is an ATPase-dependent chormatin remodeling complex, which regulates various DNA metabolic processes such as DNA replication and repair. Additionally, INO80 complex also contributes to the regulation of gene expression in sterss response and development. In order to investigate the function of INO80 complex in rhabdomyosarcoma, we examined the knockdown of subunits of INO80 complex Actr5, Ies6, and Ino80 in human rhabdomyosarcoma RD cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL20844
4 Samples
Download data: TXT
Series
Accession:
GSE169681
ID:
200169681
17.

Re-Wiring 3D Nuclear Architecture by a Single Transcription Factor during Somatic Cell Reprogramming

(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; Other; Third-party reanalysis
Platform:
GPL16791
24 Samples
Download data: BW, CSV, TXT
Series
Accession:
GSE98530
ID:
200098530
18.

MYOD Remodeling of the Genome Architecture during Myogenic Conversion of Somatic Cells

(Submitter supplied) We provide here an unprecedented analysis of the three-dimensional re-organization of the genome during cellular reprograming of one cell type into another by the ectopic expression of one single transcription factor. By integrating Hi-C analysis with ChIPseq-based detection of MYOD genome-wide binding and RNAseq profiling of gene expression, we discovered that MYOD causes profound alterations in the high order chromatin structure during fibroblast reprogramming into skeletal muscle cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Third-party reanalysis; Other
Platform:
GPL16791
16 Samples
Download data: BED, BW, CSV, NARROWPEAK, TXT
19.

MYOD Gene Expression Regulation during Myogenic Conversion of Fibroblasts

(Submitter supplied) We provide here gene expression profile of IMR90 fibroblasts expressing or not MYOD culured in GM for 1 day or GM for 1 day and DM for 3 days
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
8 Samples
Download data: BED, BW, CSV, TXT
20.

Epigenetic analysis reveals the repressive function of MyoD during myogenic differentiation

(Submitter supplied) We identify a subset of highly expressed genes related to muscle development, which show static H3K4me2 enrichment over the gene body and H3K4me3 enrichment towards the gene body during myogenic differentiation. This study reveals that MyoD significantly binds to this particular subset of genes and further systematic analysis shows the repressive role of MyoD. Interestingly, MyoD binds and down-regulates Patz1 which is important for maintaining pluripotency. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
8 Samples
Download data: BED
Series
Accession:
GSE63716
ID:
200063716
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