Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Pharmacological Repositioning of the transcription factor PU.1 [ATAC-seq]

ABSTRACT: To investigate the effects of DB2115 (PU.1 binding-site inhibitor/redistributor) upon PU.1 genomic localization, the transcriptome and chromatin accessibility.

ORGANISM(S): Homo sapiens

PROVIDER: GSE267383 | GEO | 2024/07/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Pharmacological Repositioning of the transcription factor PU.1 [ChIP-seq]

Project description:To investigate the effects of DB2115 (PU.1 binding-site inhibitor/redistributor) upon PU.1 genomic localization, the transcriptome and chromatin accessibility.

2024-07-31 | GSE267384 | GEO

Pharmacological Repositioning of the transcription factor PU.1 [CUTnTag]

Project description:This study aims to investigate the effects of PU.1 binding-site inhibitors/redistributors (DB2115, DB2373, DB2750, DB2826) upon the genomic occupancy of PU.1 and to understand DB2115-binding site preference amongst the PU.1 cistrome.

2024-07-31 | GSE267385 | GEO

Pharmacological Repositioning of the transcription factor PU.1 [CUT&TAG; CLICKonCUT&TAG]

2024-07-31 | GSE206789 | GEO

Pharmacological Repositioning of the transcription factor PU.1 [RNA-seq]

Project description:To investigate the effects of DB2115 (PU.1 binding-site inhibitor/redistributor) upon the transcriptome of the AML cell line MOLM-13.

2024-07-31 | GSE267387 | GEO

Pharmacological Repositioning of the transcription factor PU.1 [PRO-seq]

Project description:This study aims to investigate the effects of PU.1 binding-site inhibitors/redistributors (DB2115) upon nascent transcription in AML cell lines

2024-07-31 | GSE267386 | GEO

Pharmacological Repositioning of the transcription factor PU.1

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

2024-07-31 | GSE267389 | GEO

The hematopoietic master transcription factor PU.1 requires its interaction with the SWI/SNF remodeler to access chromatin de novo

Project description:PU.1 is a prototype master transcription factor (TF) of hematopoietic cell differentiation with diverse roles in different lineages. Analysis of its genome-wide binding pattern across PU.1 expressing cell types revealed manifold cell type-specific binding patterns. They are not consistent with the epigenetic and chromatin constraints to PU.1 binding observed in vitro, suggesting that PU.1 requires auxiliary factors to access DNA in vivo. Using a model of transient mRNA expression we show that PU.1 induction leads to the extensive remodeling of chromatin, redistribution of partner transcription factors and rapid initiation of a myeloid gene expression program in heterologous cell types. By probing PU.1 mutants for defects in chromatin access and screening for PU.1 proximal proteins in vivo, we found that its N-terminal acidic domain was required for the recruitment of SWI/SNF remodeling complexes, de novo chromatin access and stable binding as well as the redistribution of partner TFs.

2019-11-20 | PXD013167 | Pride

PU.1

Project description:PU.1

| PRJNA344317 | ENA

The hematopoietic master transcription factor PU.1 requires its interaction with the SWI/SNF remodeler to access chromatin de novo [ATAC-seq]

Project description:PU.1 is a prototype master transcription factor (TF) of hematopoietic cell differentiation with diverse roles in different lineages. Analysis of its genome-wide binding pattern across PU.1 expressing cell types revealed manifold cell type-specific binding patterns. They are not consistent with the epigenetic and chromatin constraints to PU.1 binding observed in vitro, suggesting that PU.1 requires auxiliary factors to access DNA in vivo. Using a model of transient mRNA expression we show that PU.1 induction leads to the extensive remodeling of chromatin, redistribution of partner transcription factors, and rapid initiation of a myeloid gene expression program in heterologous cell types. By probing mutant PU.1 variants for defects in chromatin access and screening for PU.1 proximal proteins in vivo, we found that its N-terminal acidic domain was required for the recruitment of SWI/SNF remodeling complexes, de novo chromatin access and stable binding as well as the redistribution of partner TFs.

2019-11-17 | GSE128833 | GEO

Pharmacological inhibition of the transcription factor PU.1 in leukemia.

Project description:The transcription factor PU.1 is often impaired in patients with acute myeloid leukemia (AML). Here, we used AML cells that already had low PU.1 levels and further inhibited PU.1 using either RNA interference or, to our knowledge, first-in-class small-molecule inhibitors of PU.1 that we developed specifically to allosterically interfere with PU.1-chromatin binding through interaction with the DNA minor groove that flanks PU.1-binding motifs. These small molecules of the heterocyclic diamidine family disrupted the interaction of PU.1 with target gene promoters and led to downregulation of canonical PU.1 transcriptional targets. shRNA or small-molecule inhibition of PU.1 in AML cells from either PU.1lo mutant mice or human patients with AML-inhibited cell growth and clonogenicity and induced apoptosis. In murine and human AML (xeno)transplantation models, treatment with our PU.1 inhibitors decreased tumor burden and resulted in increased survival. Thus, our study provides proof of concept that PU.1 inhibition has potential as a therapeutic strategy for the treatment of AML and for the development of small-molecule inhibitors of PU.1.

| S-EPMC5707147 | biostudies-literature

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