Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Ikaros/STAT5 DNA binding competition in pre-B cell line [ChIP-seq]

ABSTRACT: Ikaros was found to antagonize the transcriptional program of IL-7 activated pathways during pre-B cell differentiation. We analyzed the genomic distribution of Ikaros and STAT5 (downstream effector of IL-7; in the presence or absence of Ikaros) in pre-B cells by ChIP-Seq.

ORGANISM(S): Mus musculus

PROVIDER: GSE134679 | GEO | 2020/07/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Ikaros/STAT5 DNA binding competition in pre-B cell line [ChIP-seq]

Project description:Ikaros/STAT5 DNA binding competition in pre-B cell line [ChIP-seq]

| PRJNA556032 | ENA

Identification of genes controlled by Ikaros and IL-7 in the mouse Ikaros-deficient pre-B cell line BH1

Project description:The aim of the experiment was to compare to single and combined effect of Ikaros activation and IL-7 withdrawal in the Ikaros-null pre-B cell line BH1 The mouse BH1 pre-B cell line was transduced with retroviruses encoding Bcl2 and an Ikaros-estrogen receptor fusion protein. Doubly transduced cells were purified by FACS (BH1-Bcl2-Ik1ER). The transcriptome of these cells was analyzed at time 0, and after 6h and 24h of induction of Ikaros activity with 4-hydroxytamoxifen (4OHT) and/or withdrawal of IL-7. Samples from 2 independent experiments were analyzed (exp1 and exp2).

2013-11-30 | E-GEOD-51350 | biostudies-arrayexpress

Identification of genes controlled by Ikaros and IL-7 in the mouse Ikaros-deficient pre-B cell line BH1

Project description:The aim of the experiment was to compare to single and combined effect of Ikaros activation and IL-7 withdrawal in the Ikaros-null pre-B cell line BH1

2013-11-30 | GSE51350 | GEO

Ikaros target genes in pre-B cell line

Project description:We showed that the Ikaros transcription factor is essential for the pre-B cell differentiation. We analyzed the transcriptome of a Ikaros deficient pre-B cell line which was reconstituted with an inducible Ikaros-ER fusion protein. To determine the direct Ikaros targets, we did ChIP-sequencing on chromatin from this pre-B cell line, as cell numbers in mice were too limiting for these studies.

2018-05-19 | GSE114629 | GEO

STAT5 antagonism of B cell enhancer networks drives leukemia and poor patient surviva

Project description:The transcription factor STAT5 plays a critical role in B cell Acute Lymphoblastic Leukemia (B-ALL). How STAT5 mediates this effect is unclear. Here we demonstrate that STAT5 activation cooperates with defects in the pre-BCR signaling components Blnk, Btk, Prkcb, Nfkb1, and Ikzf1 to initiate B-ALL. STAT5 antagonizes NFkB and IKAROS by opposing regulation of shared target genes. STAT5 binding was enriched at super-enhancers, which were associated with an opposing network of transcription factors, including PAX5, EBF1, PU.1, IRF4, and IKAROS. Patients with high ratios of active STAT5 to NFκB or IKAROS have more aggressive disease. Our studies illustrate that an imbalance of two opposing transcriptional programs drive B-ALL, and suggest that restoring the balance of these pathways may inhibit B-ALL.

2017-04-03 | GSE86878 | GEO

Antagonism of B cell enhancer networks by STAT5 drives leukemia and poor patient survival

Project description:The transcription factor STAT5 plays a critical role in B cell acute lymphoblastic leukemia (B-ALL). How STAT5 mediates this effect is unclear. Here we demonstrate that STAT5 activation cooperates with defects in the pre-BCR signaling components encoded by Blnk, Btk, Prkcb, Nfkb1, and Ikzf1 to initiate B-ALL. STAT5 antagonizes NF-κB and IKAROS by opposing regulation of shared target genes. STAT5 binding was enriched at super-enhancers, which were associated with an opposing network of transcription factors, including PAX5, EBF1, PU.1, IRF4, and IKAROS. Patients with high ratios of active STAT5 to NF-κB or IKAROS have more aggressive disease. Our studies illustrate that an imbalance of two opposing transcriptional programs drive B-ALL, and suggest that restoring the balance of these pathways may inhibit B-ALL.

2016-11-30 | GSE25643 | GEO

Gene expression in mouse pre-B cells transduced with Ikaros.

Project description:Ikaros family DNA binding proteins are critical regulators of B cell development. To identify Ikaros-regulated genes in pre-B cells we performed gene expression studies at enhanced temporal resolution. We used retroviral gene transfer to express Ikaros proteins in the pre-B cell line B3. Total RNA from 2 biological replicates of B3 cells transduced with wild type Ikaros (HA-Ikaros-IRES-GFP) and DNA binding-deficient Ikaros mutant 159A (HA-159A Ikaros-IRES-GFP) was isolated 48h after infection. To increase the temporal resolution of Ikaros-regulated gene expression we transduced B3 cells with inducible Ikaros (HA-Ikaros-ERt2-IRES-GFP) and isolated total RNA from 3 biological replicates after 2 h and 6 h of exposure to 4-hydroxytamoxifen. Vector transduced B3 cells (ERt2-IRES-GFP) treated with 4-hydroxytamoxifen were used as controls.

2013-01-15 | E-GEOD-38110 | biostudies-arrayexpress

Gene expression in mouse primary pre-B cells transduced with Ikaros

Project description:Ikaros family DNA binding proteins are critical regulators of B cell development. To identify Ikaros-regulated genes in primary pre-B cells we performed gene expression microarrays. We used retroviral gene transfer to express Ikaros proteins. Total RNA from 3 biological replicates of primary pre-B cells transduced with wild type Ikaros (HA-Ikaros-IRES-GFP) and control vector (IRES-GFP) was isolated 48h after infection.

2013-01-15 | E-GEOD-42551 | biostudies-arrayexpress

Genome-wide identification of Ikaros binding sites in primary pre-B cells

Project description:Ikaros DNA binding proteins are important regulators of haematopoiesis and genetic deletion of Ikaros results in severe developmental disturbances, including delayed thymocyte differentiation and an early and complete block in B cell development. Although Ikaros ChIP-seq data are available for mouse thymocytes and human haematopoietic progenitors, it has not been achieved in B cell progenitors. The goal of this study was to identify Ikaros binding sites in pre-B cells to define Ikaros target genes which could explain the essential role of Ikaros proteins in B cell differentiation. We carried out chromatin immunoprecipitation and high throughput sequencing (ChIP-seq) with antibodies to the C-terminus of endogenous Ikaros in primary pre-B cells isolated from mouse fetal livers.

2013-01-15 | E-GEOD-42462 | biostudies-arrayexpress

Defining STAT5 target genes in thymic precursor cells at pre- and post-commitment stages

Project description:STAT5 is critical for inducing lineage specifying transcription factors, establishing effector gene programs, upregulating IL-2Rα (also known as CD25), and supporting cell survival in response to environmental cues in mature T cells. Although it has been shown that IL-7-induced STAT5 signaling is also essential for survival of thymic precursor cells, the exact roles of STAT5A and STAT5B and their target genes that contribute to the developmental program in early thymic development have been unknown. To define STAT5 target genes in these early T-cell progenitors, we have performed CRISPR-Cas9 mediated acute deletion of Stat5a and Stat5b in combination. We first carried out preliminary experiments to determine the stages in which IL-7 could induce maximal STAT5 phosphorylation in thymic double negative (DN) cells (B. Shin, unpublished data). We then focused on genes responding to loss of STAT5 in two different stages: CD25+ Bcl11b- pre-commitment stage, and CD25+ Bcl11b+ post-commitment stage. Of note, to generate these early pro-T cells in OP9-DLL1 coculture, we exploited bone-marrow precursor cells expressing a Bcl2 transgene to minimize survival defects due to loss of STAT5A and STAT5B. Our data show that STAT5 is necessary, in both pre- and post-commitment stages, for optimal expression of the IL-2Rα gene (Il2ra), which is constitutively expressed in normal DN2 and DN3 pro-T cells. This dataset further defines a distinct set of additional genes responding more strongly to loss of STAT5 in pro-T cells. The linked manuscript by R. Spolski et al. and other datasets referenced therein include data documenting the genomic occupancy of STAT5B in corresponding stages. In summary, our data define STAT5-responsive target genes during early T development.

2023-10-16 | GSE184845 | 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