Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Different mutant RUNX1 oncoprotein classes program alternate haematopoietic differentiation trajectories [ChIP-seq2]

ABSTRACT: Different mutant RUNX1 oncoprotein classes program alternate haematopoietic differentiation trajectories [ChIP-seq2]

PROVIDER: PRJNA647754 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12282372.fastq.gz	Fastqsanger.gz
	SRR12282373.fastq.gz	Fastqsanger.gz
	SRR12282374.fastq.gz	Fastqsanger.gz
	SRR12282375.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Different mutant RUNX1 oncoprotein classes program alternate hematopoietic differentiation trajectories

Project description:Different mutant RUNX1 oncoprotein classes program alternate hematopoietic differentiation trajectories

| PRJNA646874 | ENA

Different mutant RUNX1 oncoprotein classes program alternate haematopoietic differentiation trajectories [ChIP-seq2]

Project description:Mutations of the hematopoietic master regulator RUNX1 cause acute myeloid leukaemia, familial platelet disorder and other haematological malignancies whose phenotypes and prognoses depend on the class of RUNX1 mutation. The biochemical behaviour of these oncoproteins and their ability to cause unique diseases has been well studied but the genomic basis of their differential action is unknown. To address this question we compared integrated phenotypic, transcriptomic and genomic data from cells expressing four types of RUNX1 oncoproteins in an inducible fashion during blood development from embryonic stem cells. We show that each class of RUNX1 mutation rapidly deregulates endogenous RUNX1 function by different mechanisms, leading to specific alterations in developmentally controlled transcription factor binding and chromatin programming. The result are distinct perturbations in the trajectories of gene regulatory network changes underlying blood cell development that are consistent with the nature of the final disease phenotype. The development of novel treatments for RUNX1-driven diseases will therefore require consideration beyond RUNX1 haploinsufficiency.

2020-12-14 | GSE154858 | GEO

Different mutant RUNX1 oncoprotein classes program alternate hematopoietic differentiation trajectories [ATAC-Seq]

Project description:Different mutant RUNX1 oncoprotein classes program alternate hematopoietic differentiation trajectories [ATAC-Seq]

| PRJNA646875 | ENA

Different mutant RUNX1 oncoprotein classes program alternate hematopoietic differentiation trajectories [ChIP-Seq]

Project description:Different mutant RUNX1 oncoprotein classes program alternate hematopoietic differentiation trajectories [ChIP-Seq]

| PRJNA646876 | ENA

Different mutant RUNX1 oncoprotein classes program alternate hematopoietic differentiation trajectories [RNA-Seq]

Project description:Different mutant RUNX1 oncoprotein classes program alternate hematopoietic differentiation trajectories [RNA-Seq]

| PRJNA646877 | ENA

Different mutant RUNX1 oncoprotein classes program alternate hematopoietic differentiation trajectories [RNA-Seq]

2020-12-14 | GSE154622 | GEO

Different mutant RUNX1 oncoprotein classes program alternate hematopoietic differentiation trajectories [ChIP-Seq]

Project description:Mutations of the hematopoietic master regulator RUNX1 cause acute myeloid leukaemia, familial platelet disorder and other haematological malignancies whose phenotypes and prognoses depend on the class of RUNX1 mutation. The biochemical behavior of these oncoproteins and their ability to cause unique diseases has been well studied but the genomic basis of their differential action is unknown. To address this question we compared integrated phenotypic, transcriptomic and genomic data from cells expressing four types of RUNX1 oncoproteins in an inducible fashion during blood development from embryonic stem cells. We show that each class of RUNX1 mutation rapidly deregulates endogenous RUNX1 function by different mechanisms, leading to specific alterations in developmentally controlled transcription factor binding and chromatin programming. The result are distinct perturbations in the trajectories of gene regulatory network changes underlying blood cell development that are consistent with the nature of the final disease phenotype. The development of novel treatments for RUNX1-driven diseases will therefore require consideration beyond RUNX1 haploinsufficiency.

2020-12-14 | GSE154621 | GEO

Different mutant RUNX1 oncoprotein classes program alternate hematopoietic differentiation trajectories [ATAC-Seq]

Project description:Mutations of the hematopoietic master regulator RUNX1 cause acute myeloid leukaemia, familial platelet disorder and other haematological malignancies whose phenotypes and prognoses depend on the class of RUNX1 mutation. The biochemical behavior of these oncoproteins and their ability to cause unique diseases has been well studied but the genomic basis of their differential action is unknown. To address this question we compared integrated phenotypic, transcriptomic and genomic data from cells expressing four types of RUNX1 oncoproteins in an inducible fashion during blood development from embryonic stem cells. We show that each class of RUNX1 mutation rapidly deregulates endogenous RUNX1 function by different mechanisms, leading to specific alterations in developmentally controlled transcription factor binding and chromatin programming. The result are distinct perturbations in the trajectories of gene regulatory network changes underlying blood cell development that are consistent with the nature of the final disease phenotype. The development of novel treatments for RUNX1-driven diseases will therefore require consideration beyond RUNX1 haploinsufficiency.

2020-12-14 | GSE154620 | GEO

Different mutant RUNX1 oncoprotein classes program alternate hematopoietic differentiation trajectories

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-12-14 | GSE154623 | GEO

A trio of bipotent precursors seeds the mesenchymal, haematopoietic, and endothelial lineages of the yolk sac

Project description:During embryogenesis, haematopoietic and endothelial lineages emerge closely in time and space. It is thought that the first blood and endothelium derive from a common clonal ancestor, the haemangioblast. However, investigation of candidate haemangioblasts in vitro has revealed a mesenchymal differentiation potential, a feature more compatible with an earlier mesodermal precursor. To date, no evidence for an in vivo haemangioblast has been discovered. Using single cell RNA-Sequencing and in vivo cellular barcoding, we have unraveled the ancestral relationships that give rise to the haematopoietic lineages of the yolk sac, the endothelium, and the mesenchyme. We show that the mesodermal derivatives of the yolk sac are produced by three distinct bipotential precursors: the haemangioblast, mesenchymoangioblast, and a novel cell type: the haematomesoblast. Between E6.5 and E7.5, this trio of precursors seeds haematopoietic, endothelial, and mesenchymal trajectories.

2022-12-21 | GSE204896 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data