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Links from GEO DataSets

Items: 20

1.

CASZ1 directly regulates expression of myogenic genes through regional epigenetic modifications to induce muscle and rhabdomyosarcoma cell differentiation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
6 related Platforms
57 Samples
Download data: BW
Series
Accession:
GSE126147
ID:
200126147
2.

RNA-sequencing analysis to investigate genes regulated by CASZ1 in RD cells

(Submitter supplied) In this study we identified genes regulated by CASZ1b in RD cells
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
6 Samples
Download data: TXT
3.

RNA-sequencing analysis to investigate genes regulated by CASZ1 in SMS-CTR cells

(Submitter supplied) In this study we identified genes regulated by CASZ1b in SMS-CTR cells
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
10 Samples
Download data: TXT
4.

RNA-sequencing analysis to investigate genes regulated by CASZ1 in C2C12 cells

(Submitter supplied) In this study we identified genes regulated by CASZ1b in C2C12 cells
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL21493 GPL21103
15 Samples
Download data: TXT
Series
Accession:
GSE126144
ID:
200126144
5.

Genome-wide mapping of CASZ1 binding sites in differentiated SMS-CTR cells [Trametinib]

(Submitter supplied) MEK inhibitor trametinib induces SMS-CTR cell differentiation and up-regulates CASZ1 expression. We identified genome-wide binding sites of CASZ1 in differentiated SMS-CTR cells.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
4 Samples
Download data: BW
Series
Accession:
GSE126143
ID:
200126143
6.

Genome-wide mapping of CASZ1b binding sites and investigate its effect on chromatin status in SMS-CTR cells [CTRtetCASZ1b]

(Submitter supplied) In SMS-CTR cells, we identified genomewide binding sites of CASZ1b. The overexpression of CASZ1b in SMS-CTR cells led to a regional epigenetic modification.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
14 Samples
Download data: BW
Series
Accession:
GSE126142
ID:
200126142
7.

The affect of loss of Casz1 in C2C12 cells on super-enhancers

(Submitter supplied) In the differereniated C2C12 cells, knockdown of Casz1 leads to a re-establishment of super-enhancers
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
6 Samples
Download data: BW
Series
Accession:
GSE126141
ID:
200126141
8.

Investigate the affect of CASZ1b on chromatin accessibility in SMS-CTR cells

(Submitter supplied) In SMS-CTR cells, the overexpression of CASZ1b in SMS-CTR cells led to a modification of regional chromation accessibility.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
2 Samples
Download data: BW
Series
Accession:
GSE126140
ID:
200126140
9.

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
10.

Genome-wide maps of Twist2-binding, MyoD-binding and chromatin state in Twist2-overexpressing Twist2+ cells

(Submitter supplied) Integrated analysis of genome-wide ChIP-Seq and RNA-Seq data revealed the first dynamic chromatin and transcriptional landscape of Twist2 binding during myogenic differentiation. During differentiation, Twist2 competes with MyoD at shared DNA motifs to direct global gene transcription and repression of the myogenic program. Additionally, TWIST2 shapes the epigenetic landscape to drive chromatin opening at oncogenic loci and chromatin closing at myogenic loci. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
34 Samples
Download data: BIGWIG
Series
Accession:
GSE127998
ID:
200127998
11.

The Hippo tranducer YAP1 transforms activated satellite cells and is a potent effector of embryonal rhabdomyosarcoma formation

(Submitter supplied) The Hippo pathway effector YAP1 controls stem cell fate in epithelial tissues, but its role in stem cells of non-epithelial tissues, such as skeletal muscle, is poorly documented. Here we show that sustained YAP1 activity in mouse activated satellite cells in vivo induces rhabdomyosarcoma (RMS) resembling human embryonal RMS (ERMS) with high penetrance and short latency. The transcriptional program of YAP1 in ERMS drives pro-proliferative pathways whilst decreasing MyoD1 and MEF2 pro-differentiation activity to globally maintain the myoblastic phenotype of ERMS. more...
Organism:
Homo sapiens; Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL13112 GPL11154
4 Samples
Download data: BED
Series
Accession:
GSE55186
ID:
200055186
12.

Role of Yes-Associated Protein 1 (YAP1) in rhabdomyosarcoma

(Submitter supplied) Doxycycline-inducible YAP1 S127A-driven rhabdomyosarcoma (RMS) tumors, control skeletal muscle and regressed tumors following YAP1 normalization by doxycycline withdrawal were compared to determine the YAP1-regulated gene expression profile relevant to RMS formation. To characterize the role of YAP1 in embryonal RMS at the molecular level and identify a gene signature for YAP1 activity readout, we compared the gene expression profiles of our YAP1-driven ERMS with control donor skeletal muscle (SKM) and doxycycline-withdrawn regressing tumors by microarray (doxycycline withdrawal for 3 or 6 days; OFF3 and OFF6, respectively). more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
12 Samples
Download data: CEL
Series
Accession:
GSE47198
ID:
200047198
13.

RNA-Seq and ChIP-Seq in SIX1 deficient Rhabdomyosarcoma cells

(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
Platforms:
GPL24676 GPL18573
21 Samples
Download data: TDF
Series
Accession:
GSE173155
ID:
200173155
14.

Chromatin states and transcription factor binding in SIX1 deficient Rhabdomyosarcoma cells

(Submitter supplied) Genetic and shRNA-mediated inhibition of SIX1 expression in RMS cells induces myogenic differentiation and impedes RMS tumor growth. To elucidate the mechanism by which SIX1 loss activates a differentiation program, we performed SIX1, MYOD1, and H3K27ac ChIPseq in two SIX1 knockdown SMS-CTR cell lines and one control SMS-CTR cell line to profile changes in transcriptional activity and myogenic transcription factor binding in fusion-negative Rhabdomyosarcoma.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
12 Samples
Download data: TDF
Series
Accession:
GSE173151
ID:
200173151
15.

Transcriptomes of SIX1 deficient and control Rhabdomyosarcoma cells

(Submitter supplied) Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived retinal transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis Genetic and shRNA-mediated inhibition of SIX1 expression in RMS cells induces myogenic differentiation and impedes RMS tumor growth. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
9 Samples
Download data: 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.

Epigenetic Reprogramming of mutant RAS-driven Rhabdomyosarcoma via MEK Inhibition

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by array; Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL1261 GPL11154
60 Samples
Download data: BED, CEL, FPKM_TRACKING
Series
Accession:
GSE85171
ID:
200085171
18.

MEK inhibition rewires enhancer landscapes in RAS-driven Rhabdomyosarcoma to unlock a myogenic differentation block

(Submitter supplied) Trametinib-treated rhabdomyosarcoma cells undergo transcriptional reprogramming akin to myogenic differentiation. This reprogramming is induced by loss of ERK-mediated inhibition of MYOG expression. Restoration of MYOG allows establishment of super-enhancers at genes expressed by terminally differentiated myotubes. Our findings demonstrate that aberrant MAP kinase activity blocks differentiation in rhabdomyosarcoma and highlight trametinib as a potential therapeutic for RAS-mutated rhabdomyosarcoma.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
18 Samples
Download data: FPKM_TRACKING
19.

MEK inhibition profoundly reprograms myogenic super enhancers in mutant-RAS driven Rhabdomyosarcoma

(Submitter supplied) Trametinib-treated rhabdomyosarcoma cells undergo transcriptional reprogramming akin to myogenic differentiation. This reprogramming is induced by loss of ERK-mediated inhibition of MYOG expression. Restoration of MYOG allows establishment of super-enhancers at genes expressed by terminally differentiated myotubes. Our findings demonstrate that aberrant MAP kinase activity blocks differentiation in rhabdomyosarcoma and highlight trametinib as a potential therapeutic for RAS-mutated rhabdomyosarcoma.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11154 GPL18573
38 Samples
Download data: BED
Series
Accession:
GSE85169
ID:
200085169
20.

Oncogenic RAS blocks myogenic differentiation

(Submitter supplied) C2C12 mouse myoblasts expressing RAS mutants identified in human tumors fail to differentiate in low serum media.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
4 Samples
Download data: CEL
Series
Accession:
GSE85168
ID:
200085168
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