Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

41 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CCAAT/enhancer-binding protein alpha target genes in myeloid progenitor cells uncovered by chromatin IP

ABSTRACT: CCAAT/enhancer-binding protein alpha (C/EBPM-NM-1) is a lineage-specific transcription factor that directs development of granulocytes. To obtain insights into the genome-wide transcriptome of wild type C/EBPM-NM-1, we have performed chromatin immunoprecipitation on DNA promoter microarrays (ChIP-chip) in the murine 32D myeloid progenitor cell line. These cells expressed an estradiol-inducible form of wild-type C/EBPM-NM-1. In the murine 32D myeloid progenitor cell line, expressing either an estradiol-inducible form of wild-type C/EBPM-NM-1. (C/EBPM-NM-1-ER, n=3, replicates), or as a control ER (n=2, replicates), we have performed chromatin immunoprecipitation on DNA promoter microarrays (ChIP-chip) after 4 hours of estradiol incubation.

ORGANISM(S): Mus musculus

SUBMITTER: Erdogan Taskesen

PROVIDER: E-GEOD-19321 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

HAT: hypergeometric analysis of tiling-arrays with application to promoter-GeneChip data.

Taskesen Erdogan E Beekman Renee R de Ridder Jeroen J Wouters Bas J BJ Peeters Justine K JK Touw Ivo P IP Reinders Marcel J T MJ Delwel Ruud R

BMC bioinformatics 20100521

<h4>Background</h4>Tiling-arrays are applicable to multiple types of biological research questions. Due to its advantages (high sensitivity, resolution, unbiased), the technology is often employed in genome-wide investigations. A major challenge in the analysis of tiling-array data is to define regions-of-interest, i.e., contiguous probes with increased signal intensity (as a result of hybridization of labeled DNA) in a region. Currently, no standard criteria are available to define these region ...[more]

PMID: 20492700

Similar Datasets

Mutant-CCAAT/enhancer-binding protein alpha target genes in myeloid progenitor cells by chromatin IP

Project description:CCAAT/enhancer-binding protein alpha (C/EBPM-NM-1) is a lineage-specific transcription factor that directs development of granulocytes. To obtain insights into the genome-wide transcriptome of mutant C/EBPM-NM-1, we have performed chromatin immunoprecipitation on DNA promoter microarrays (ChIP-chip) in the murine 32D myeloid progenitor cell line. These cells expressed an estradiol-inducible form of mutant C/EBPM-NM-1. In the murine 32D myeloid progenitor cell line, expressing an estradiol-inducible form of C-terminal mutant of C/EBPM-NM-1. (n=2, replicates). We have performed chromatin immunoprecipitation on DNA promoter microarrays (ChIP-chip) after 4 hours of estradiol incubation.

2013-12-01 | E-GEOD-36268 | biostudies-arrayexpress

Gene expression profiling of C/EBPM-NM-2- and STAT3-deficient human endometrial stromal cells (HESC)

Project description:Our previous studies have shown that C/EBPM-NM-2 plays a critical role in human endometrial stromal decidualization. In order to identify the molecular pathways regulated by C/EBPM-NM-2 during decidualization, we performed gene expression profiling using RNA isolated from normal and C/EBPM-NM-2-deficient human endometrial stromal cells. The microarray results revealed that several key regulators of stromal differentiation, such as BMP2, Wnt4, IL-11RM-NM-1 and STAT3, operate downstream of C/EBPM-NM-2 during decidualization. Further studies revealed that STAT3 is a direct target of C/EBPM-NM-2 and plays an important role in cytokine signal during the decidualization process. Gene expression profiling, using STAT3-deficient HESCs, showed an extensive overlap of pathways downstream of STAT3 and C/EBPM-NM-2 during stromal cell differentiation. We employed a siRNA strategy to suppress C/EBPM-NM-2 or STAT3 mRNA expression in HESCs and then performed microarray analysis to identify its downstream target genes. Further, using a similar strategy, we focused on STAT3, a C/EBPM-NM-2 target gene, and identified the commone pathways downstream of both C/EBPM-NM-2 and STAT3.

2012-10-11 | E-GEOD-41473 | biostudies-arrayexpress

FOXP3 binding sites in promoter regions of human Jurkat T cells

Project description:The transcription factor (TF) Forkhead Box P3 (FOXP3) is constitutively expressed in high levels in natural occurring CD4+CD25+ regulatory T cells (nTreg) and is not only the most accepted marker for that cell population, but is considered lineage determinative. Chromatin immunoprecipitation (ChIP) of transcription factors in combination with genomic tiling microarray analysis (ChIP-on-Chip) has been shown to be an appropriate tool to identify FOXP3 transcription factor binding sites (TFBS) on a genome-wide scale. In combination with microarray expression analysis the ChIP-on-Chip technique allows to identify direct FOXP3 target genes. ChIP-on-Chip analysis of human FOXP3M-NM-^T2 isoform expressed in resting and PMA / ionomycin stimulated Jurkat T cells revealed several thousand putative FOXP3 binding sites and importance of intronic regions for FOXP3 binding. Knowledge of general distribution patterns of FOXP3 TFBS in the human genome under resting and activated conditions contributes to a better understanding of this TF and its influence on direct target genes with importance for Treg cell phenotype and function. ChIP-DNA from FOXP3(M-NM-^T2) expressing Jurkat T cells under resting and PMA / ionomycin stimulated conditions from duplicate experiments was analyzed. FOXP3-specific tiling array data were analyzed in reference to an individual isotype control dataset (J-FOXP3 ChIP'd with FOXP3 antibody vs. J-FOXP3 ChIP'd with isotype control antibody). In total 8 tiling array analyses were performed (2x resting J-FOXP3 with FOXP3-IP, 2x resting J-FOXP3 with isotype-IP, 2x PMA/iono J-FOXP3 with FOXP3-IP, 2x PMA/iono J-FOXP3 with isotype-IP)

2012-11-26 | E-GEOD-37252 | biostudies-arrayexpress

ChIP-chip analysis of GBF1 in the presence and absence of its heterodimerizing partners, HY5 and HYH

Project description:Transcription factors are key components of light signalling as they amplify the signal, which results in massive changes in genome-wide expression during photomorphogenesis. Three bZIP transcription factors (TFs), namely GBF1, HY5, and HYH, form heterodimers with each other and regulate photomorphogenesis in an interdependent manner. GBF1 acts as both a positive and negative regulator of photomorphogenesis, whereas HY5 and HYH mainly act as positive regulators of photomorphogenesis. In this study, the impact of heterodimerization of GBF1 with HY5 and HYH was analyzed for genome-wide binding of GBF1 through ChIP-chip in GBF1. We identified more than 2000 direct targets of GBF1 in the presence of HY5 and HYH. However, in the absence of HY5, very few binding sites were found, and in the absence of functional HYH protein, the number of GBF1 direct targets reduced to only half compared to when functional HYH was present. ChIPed DNA with GBF1 antibody from GBF1OE, hy5 GBF1OE, and hyh GBF1OE lines vs. ChIPed DNA with GBF1 antibody from wild-type.

2014-03-24 | E-GEOD-36965 | biostudies-arrayexpress

Heterodimerization of GBF1 with HY5 and HYH is crucial for its genome wide binding and target gene regulation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-03-24 | E-GEOD-49337 | biostudies-arrayexpress

Usf1, a Suppressor of the Circadian Clock Mutant, Reveals the Nature of the DNA-binding of the CLOCK:BMAL1 complex in mice

Project description:Genetic and molecular approaches have been critical for elucidating the mechanism of the mammalian circadian clock. Here, we demonstrate that the ClockM-NM-^T19 mutant behavioral phenotype is significantly modified by mouse strain genetic background. We map a suppressor of the ClockM-NM-^T19 mutation to a M-bM-^HM-<900 kb interval on mouse chromosome 1 and identify the transcription factor, Usf1, as the responsible gene. A SNP in the promoter of Usf1 causes elevation of its transcript and protein in strains that suppress the Clock mutant phenotype. USF1 competes with the CLOCK:BMAL1 complex for binding to E-box sites in target genes. Saturation binding experiments demonstrate reduced affinity of the CLOCKM-NM-^T19:BMAL1 complex for E-box sites, thereby permitting increased USF1 occupancy on a genome-wide basis. We propose that USF1 is an important modulator of molecular and behavioral circadian rhythms in mammals. DOI:http://dx.doi.org/10.7554/eLife.00426.001. Examination of 3 transcriptional regulators in mouse liver at ZT8

2013-04-21 | E-GEOD-44609 | biostudies-arrayexpress

Deregulation of the endogenous C/EBPM-NM-2 LIP isoform predisposes to tumorigenesis

Project description:Two long and one truncated isoforms (termed LAP*, LAP, and LIP, respectively) of the transcription factor CCAAT enhancer binding protein beta (C/EBPM-NM-2) are expressed from a single intronless Cebpb gene by alternative translation initiation. Isoform expression is sensitive to mammalian target of rapamycin (mTOR)-mediated activation of the translation initiation machinery and relayed through an upstream open reading frame (uORF) on the C/EBPM-NM-2 mRNA. The truncated C/EBPM-NM-2 LIP, initiated by high mTOR activity, has been implied in neoplasia, but it was never shown whether endogenous C/EBPM-NM-2 LIP may function as an oncogene. In this study, we examined spontaneous tumor formation in C/EBPM-NM-2 knockin mice that constitutively express only the C/EBPM-NM-2 LIP isoform from its own locus. Our data show that deregulated C/EBPM-NM-2 LIP predisposes to oncogenesis in many tissues. Gene expression profiling suggests that C/EBPM-NM-2 LIP supports a protumorigenic microenvironment, resistance to apoptosis, and alteration of cytokine/chemokine expression. The results imply that enhanced translation reinitiation of C/ EBPM-NM-2 LIP promotes tumorigenesis. Accordingly, pharmacological restriction of mTOR function might be a therapeutic option in tumorigenesis that involves enhanced expression of the truncated C/EBPM-NM-2 LIP isoform. A cohort of C/EBPb LIP heterozygous (+/L) and wild type (+/+) mice were kept over 25 months and animals showing palpable lymphoma were sacrificed. The lymphoma developed spontaneously. For each genotype, 5 lymphoma were used for RNA preparation and gene expression profiling analysis.

2014-12-16 | E-GEOD-53770 | biostudies-arrayexpress

The p23 molecular chaperone and GCN5 acetylase jointly modulate protein-DNA dynamics and open chromatin status.

Project description:Dense mapping of individual DNase I cleavages from intact nuclei isolated from wild type, sba1M-NM-^T and gcn5M-NM-^T yeast using high-throughput sequencing. Open chromatin status of wild type, sba1-/- and gcn5-/- yeast strains were generated by Dnase-seq.

2012-08-23 | E-GEOD-40255 | biostudies-arrayexpress

C/EBPM-NM-1 poises B cells for rapid reprogramming into iPS cells

Project description:C/EBPM-NM-1 induces transdifferentiation of B cells into macrophages at high efficiencies and enhances reprogramming into induced pluripotent stem cells (iPSCs) when co-expressed with Oct4, Sox2, Klf4 and Myc (OSKM). However, how C/EBPM-NM-1 accomplishes these effects is unclear. We now found that transient C/EBPM-NM-1 expression followed by OSKM activation induces a 100 fold increase in iPSC reprogramming efficiency, involving 95% of the cells. During this conversion pluripotency and epithelial-mesenchymal transition genes become dramatically up-regulated and 60% of the cells express Oct4 within 2 days. C/EBPM-NM-1 acts as a pathbreaker since it transiently makes the chromatin of pluripotency genes more accessible to DNase I. It also induces the expression of the dioxygenase Tet2 and promotes its translocation to the nucleus where it binds to regulatory regions of pluripotency genes that become demethylated following OSKM induction. In line with these findings, overexpression of Tet2 enhances OSKMM-bM-^@M-^Pinduced B cell reprogramming. Since the enzyme is also required for efficient C/EBPM-NM-1-induced immune cell conversion, our data suggest that Tet2 provides a mechanistic link between iPSC reprogramming and B cell transdifferentiation. The rapid iPS reprogramming approach described should help to fully elucidate the process and has potential clinical applications. Refer to individual Series

2013-11-17 | E-GEOD-52397 | biostudies-arrayexpress

RUNX1 reshapes the epigenetic landscape at the onset of hematopoiesis

Project description:Cell fate decisions during hematopoiesis are governed by lineage-specific transcription factors, such as RUNX1, SCL/TAL1, FLI1 and C/EBP family members. In order to gain insight about how these transcription factors regulate the activation of hematopoietic genes during embryonic development, we measured the genome-wide dynamics of transcription factor assembly on their target genes during the RUNX1-dependent transition from hemogenic endothelium to hematopoietic progenitors. Using a RUNX1-/- embryonic stem cell differentiation model expressing an inducible RUNX1 gene, we show that in the absence of RUNX1, SCL/TAL1, FLI1 and C/EBPM-NM-2 prime hematopoietic genes and that this early priming is required for correct temporal expression of the myeloid master regulator PU.1 and its downstream targets. After induction, RUNX1 binds to numerous new sites, initiating a local increase of histone acetylation and rapid global alterations in the binding patterns of SCL/TAL1 and FLI1. The acquisition of hematopoietic fate controlled by RUNX1 therefore does not represent the establishment of a new regulatory layer on top of a pre-existing hemogenic endothelium program but instead entails global reorganization of lineage-specific transcription factor assemblies. ChIPseq data from transcription factors Runx1, Fli-1, Scl/Tal1 and C/EBPM-NM-2, histone modification H3K9Ac as well as RNA Pol II obtained from differentiating murine hematopoietic cells

2012-10-18 | E-GEOD-40235 | biostudies-arrayexpress

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