Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE236775 | GEO | 2023/11/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth.

Project description:AML is a heterogenous disease caused by different mutations. We have previously shown that each mutational sub-type develops its specific gene regulatory network (GRN) with transcription factors interacting with multiple gene modules, many of which are transcription factor genes themselves. Here we hypothesized that highly connected nodes within such networks comprise crucial regulators of AML maintenance. We tested this hypothesis using FLT3-ITD mutated AML as a model and conducted an shRNA drop-out screen informed by this analysis. We show that AML-specific GRNs predict identifying crucial regulatory modules required for AML but not normal cellular growth. Furthermore, our work shows that all modules are highly connected and regulate each other. The careful multi-omic analysis of the role of one (RUNX1) module by shRNA and chemical inhibition shows that this transcription factor and its target genes stabilize the GRN of FLT3-ITD AML and that its removal leads to GRN collapse and cell death.

| S-EPMC10370108 | biostudies-literature

Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth [shRNA-seq]

Project description:AML is a heterogenous disease caused by different mutations. We have previously shown that each mutational sub-type develops its specific gene regulatory network (GRN) with transcription factors interacting with multiple gene modules, many of which are transcription factor genes themselves. Here we hypothesized that highly connected nodes within such networks comprise crucial regulators of AML maintenance. We tested this hypothesis using FLT3-ITD mutated AML as model and conducted an shRNA drop-out screen informed by this analysis. Our screen showed that AML-specific GRNs are predictive for identifying crucial regulatory modules required for AML but not normal cellular growth. Furthermore, our work shows that all modules are highly connected and regulate each other. The careful multi-omic analysis of the role of one (RUNX1) module by shRNA and chemical inhibition shows that this transcription factor and its target genes stabilize the GRN of FLT3-ITD AML and that its removal leads to GRN collapse and cell death

2023-11-20 | GSE236774 | GEO

Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth [scRNA-seq]

Project description:AML is a heterogenous disease caused by different mutations. We have previously shown that each mutational sub-type develops its specific gene regulatory network (GRN) with transcription factors interacting with multiple gene modules, many of which are transcription factor genes themselves. Here we hypothesized that highly connected nodes within such networks comprise crucial regulators of AML maintenance. We tested this hypothesis using FLT3-ITD mutated AML as model and conducted an shRNA drop-out screen informed by this analysis. Our screen showed that AML-specific GRNs are predictive for identifying crucial regulatory modules required for AML but not normal cellular growth. Furthermore, our work shows that all modules are highly connected and regulate each other. The careful multi-omic analysis of the role of one (RUNX1) module by shRNA and chemical inhibition shows that this transcription factor and its target genes stabilize the GRN of FLT3-ITD AML and that its removal leads to GRN collapse and cell death

2023-11-20 | GSE236773 | GEO

Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth [ATAC-seq]

Project description:AML is a heterogenous disease caused by different mutations. We have previously shown that each mutational sub-type develops its specific gene regulatory network (GRN) with transcription factors interacting with multiple gene modules, many of which are transcription factor genes themselves. Here we hypothesized that highly connected nodes within such networks comprise crucial regulators of AML maintenance. We tested this hypothesis using FLT3-ITD mutated AML as model and conducted an shRNA drop-out screen informed by this analysis. Our screen showed that AML-specific GRNs are predictive for identifying crucial regulatory modules required for AML but not normal cellular growth. Furthermore, our work shows that all modules are highly connected and regulate each other. The careful multi-omic analysis of the role of one (RUNX1) module by shRNA and chemical inhibition shows that this transcription factor and its target genes stabilize the GRN of FLT3-ITD AML and that its removal leads to GRN collapse and cell death

2023-11-20 | GSE236770 | GEO

Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth [RNA-seq]

Project description:AML is a heterogenous disease caused by different mutations. We have previously shown that each mutational sub-type develops its specific gene regulatory network (GRN) with transcription factors interacting with multiple gene modules, many of which are transcription factor genes themselves. Here we hypothesized that highly connected nodes within such networks comprise crucial regulators of AML maintenance. We tested this hypothesis using FLT3-ITD mutated AML as model and conducted an shRNA drop-out screen informed by this analysis. Our screen showed that AML-specific GRNs are predictive for identifying crucial regulatory modules required for AML but not normal cellular growth. Furthermore, our work shows that all modules are highly connected and regulate each other. The careful multi-omic analysis of the role of one (RUNX1) module by shRNA and chemical inhibition shows that this transcription factor and its target genes stabilize the GRN of FLT3-ITD AML and that its removal leads to GRN collapse and cell death

2023-11-20 | GSE236772 | GEO

Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth [ChIP-seq]

Project description:AML is a heterogenous disease caused by different mutations. We have previously shown that each mutational sub-type develops its specific gene regulatory network (GRN) with transcription factors interacting with multiple gene modules, many of which are transcription factor genes themselves. Here we hypothesized that highly connected nodes within such networks comprise crucial regulators of AML maintenance. We tested this hypothesis using FLT3-ITD mutated AML as model and conducted an shRNA drop-out screen informed by this analysis. Our screen showed that AML-specific GRNs are predictive for identifying crucial regulatory modules required for AML but not normal cellular growth. Furthermore, our work shows that all modules are highly connected and regulate each other. The careful multi-omic analysis of the role of one (RUNX1) module by shRNA and chemical inhibition shows that this transcription factor and its target genes stabilize the GRN of FLT3-ITD AML and that its removal leads to GRN collapse and cell death

2023-11-20 | GSE236771 | GEO

Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth.

Project description:Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth.

| PRJNA992405 | ENA

Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth [ATAC-seq]

Project description:Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth [ATAC-seq]

| PRJNA992410 | ENA

Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth [ChIP-seq]

Project description:Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth [ChIP-seq]

| PRJNA992411 | ENA

Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth [scRNA-seq]

Project description:Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth [scRNA-seq]

| PRJNA992414 | ENA

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