Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

ABSTRACT: RUNX1-ETO and RUNX1-EVI-1 differentially program the chromatin landscape in t(3 21) and t(8 21) AML but share global C/EBP-alpha dysfunction (DNase-Seq)

PROVIDER: PRJNA343969 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR4291620.fastq.gz	Fastqsanger.gz
	SRR4291621.fastq.gz	Fastqsanger.gz
	SRR4291612.fastq.gz	Fastqsanger.gz
	SRR4291622.fastq.gz	Fastqsanger.gz
	SRR4291613.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 11

Similar Datasets

RUNX1-ETO and RUNX1-EVI-1 differentially program the chromatin landscape in t(3 21) and t(8 21) AML but share global C/EBP-alpha dysfunction

Project description:RUNX1-ETO and RUNX1-EVI-1 differentially program the chromatin landscape in t(3 21) and t(8 21) AML but share global C/EBP-alpha dysfunction

| PRJNA343965 | ENA

Homo sapiens

Project description:RUNX1-ETO and RUNX1-EVI-1 differentially program the chromatin landscape in t(3 21) and t(8 21) AML but share global C/EBP-alpha dysfunction (RNA-Seq)

| PRJNA343968 | ENA

Homo sapiens

Project description:RUNX1-ETO and RUNX1-EVI-1 differentially program the chromatin landscape in t(3 21) and t(8 21) AML but share global C/EBP-alpha dysfunction (ChIP-Seq)

| PRJNA343970 | ENA

RUNX1-ETO and RUNX1-EVI-1 differentially program the chromatin landscape in t(3;21) and t(8;21) AML but share global C/EBP-alpha dysfunction (RNA-Seq)

Project description:RUNX1 is a frequent target of translocations in acute myeloid leukemia whereby its DNA binding domain fuses to different epigenetic regulators. To assess how different RUNX1 fusion proteins interact with the epigenome we compared the global binding patterns and the chromatin landscape of t(8;21) and t(3;21) AML which express RUNX1-ETO and RUNX1-EVI-1, respectively. We found that differential prognosis for these types of AML is reflected in fundamental differences in gene expression, chromatin landscape, binding patterns of the fusion proteins and other transcription factors as identified by genome-wide digital footprinting in patients. As previously shown for RUNX1-ETO, knockdown of RUNX1-EVI-1 expression initiates differentiation of t(3;21) cells which is associated with up-regulation of genes vital for myeloid differentiation, including C/EBPα. Furthermore, by expressing either dominant-negative C/EBP or an inducible C/EBPα construct in t(3;21) cells we show that C/EBPα is necessary and sufficient for the differentiation response of these cells to RUNX1-EVI-1 knockdown.

2017-06-26 | GSE87285 | GEO

RUNX1-ETO and RUNX1-EVI-1 differentially program the chromatin landscape in t(3;21) and t(8;21) AML but share global C/EBP-alpha dysfunction (DNase-Seq)

2017-06-26 | GSE87284 | GEO

RUNX1-ETO and RUNX1-EVI-1 differentially program the chromatin landscape in t(3;21) and t(8;21) AML but share global C/EBP-alpha dysfunction (ChIP-Seq)

2017-06-26 | GSE87283 | GEO

Identification of a dynamic core transcriptional network in t(8;21) AML regulating differentiation block and self-renewal [ChIP-Seq]

Project description:The leukemogenic fusion protein RUNX1/ETO impairs myeloid differentiation and drives malignant self-renewal. Here we use digital footprinting and ChIP-sequencing to identify the core RUNX1/ETO responsive transcriptional network of t(8;21) cells. We show that the transcriptional programme underlying leukemic propagation is regulated by a dynamic equilibrium between RUNX1/ETO and RUNX1 complexes, which bind in a mutually exclusive fashion to identical genomic sites. Perturbation of this equilibrium by RUNX1/ETO knockdown results in a global reassembly of transcription factor complexes within pre-existing open chromatin and the formation of a new C/EBP-alpha-dominated transcriptional network driving myeloid differentiation. Our work demonstrates that the block in myeloid differentiation in t(8;21) is caused by the dynamic balance between RUNX1/ETO and RUNX1 activities and the repression of C/EBP-alpha and highlights the core targets of epigenetic reprogramming in t(8;21) AML. ChIP-sequencing and DNAse1-sequencing was used for the identification of a dynamic core transcriptional network in t(8;21) AML

2014-09-24 | E-GEOD-60130 | biostudies-arrayexpress

Identification of a dynamic core transcriptional network in t(8;21) AML regulating differentiation block and self-renewal [RNA-Seq]

Project description:The leukemogenic fusion protein RUNX1/ETO impairs myeloid differentiation and drives malignant self-renewal. Here we use digital footprinting and ChIP-sequencing to identify the core RUNX1/ETO responsive transcriptional network of t(8;21) cells. We show that the transcriptional programme underlying leukemic propagation is regulated by a dynamic equilibrium between RUNX1/ETO and RUNX1 complexes, which bind in a mutually exclusive fashion to identical genomic sites. Perturbation of this equilibrium by RUNX1/ETO knockdown results in a global reassembly of transcription factor complexes within pre-existing open chromatin and the formation of a new C/EBP-dominated transcriptional network driving myeloid differentiation. Our work demonstrates that the block in myeloid differentiation in t(8;21) is caused by the dynamic balance between RUNX1/ETO and RUNX1 activities and the repression of C/EBP and highlights the core targets of epigenetic reprogramming in t(8;21) AML. ChIP-sequencing, DNAse1-sequencing and RNA-sequncing was used for the identification of a dynamic core transcriptional network in t(8;21) AML This submission represents the RNA-Seq component of the study

2014-09-24 | E-GEOD-54478 | biostudies-arrayexpress

Identification of a dynamic core transcriptional network in t(8;21) AML regulating differentiation block and self-renewal [RNA-Seq]

Project description:The leukemogenic fusion protein RUNX1/ETO impairs myeloid differentiation and drives malignant self-renewal. Here we use digital footprinting and ChIP-sequencing to identify the core RUNX1/ETO responsive transcriptional network of t(8;21) cells. We show that the transcriptional programme underlying leukemic propagation is regulated by a dynamic equilibrium between RUNX1/ETO and RUNX1 complexes, which bind in a mutually exclusive fashion to identical genomic sites. Perturbation of this equilibrium by RUNX1/ETO knockdown results in a global reassembly of transcription factor complexes within pre-existing open chromatin and the formation of a new C/EBP-dominated transcriptional network driving myeloid differentiation. Our work demonstrates that the block in myeloid differentiation in t(8;21) is caused by the dynamic balance between RUNX1/ETO and RUNX1 activities and the repression of C/EBP and highlights the core targets of epigenetic reprogramming in t(8;21) AML.

2014-09-24 | GSE54478 | GEO

Identification of a dynamic core transcriptional network in t(8;21) AML regulating differentiation block and self-renewal [ChIP-Seq]

2014-09-24 | GSE60130 | GEO