Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

9 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ChIPseq of Myocyte Enhancer Factor 2 in neonatal rat cardiomyocytes to distinguish MEF2 binding sites

ABSTRACT: Myocyte enhancer factor 2 contributes as a transcription factor to cardiac remodeling processes. We wanted to link and compare known myocyte enhancer factor 2 targets to overall targets. Therefore, we used a model of neonatal rat cardiomyocytes and precipitated sheared chromatin samples with 5µg of MEF2 Ab.

INSTRUMENT(S): Illumina HiSeq 2000

ORGANISM(S): Rattus norvegicus

SUBMITTER: Lorenz Lehmann

PROVIDER: E-MTAB-6213 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Identification of MEF2 binding sites in adult mouse ventricular myocytes

Project description:The experiment was designed to assess genome-wide binding sites of Myocyte Enhancer Factor 2 (MEF2) in adult mouse ventricular cardiomyocytes.

2021-09-15 | E-MTAB-9146 | biostudies-arrayexpress

Identification of histone modifications in cardiomyocytes of conditional HDAC4 knockout mice

Project description:Histone Deacetylase 4 (HDAC4) is known to contribute to cardiac remodeling processes. We wanted to identify and compare different genome wide targets of HDAC4 to well described interaction partners and its functional consequences. Therefore, we used a model of adult cardiomyocytes isolated from HDAC4 knockout mice and Wildtyp (WT) controls. We looked for HDAC4s contribution to changes of activating histone modifications (H3K4me3, H3K9ac, H3K27ac) and repressive pendants (H3K9me2 and H3K27me3).

2021-09-15 | E-MTAB-7319 | biostudies-arrayexpress

Identification of CaMKII-dependent H3S28p target genes

Project description:To identify direct CaMKII-dependent downstream genes of H3S28p we used chromatin-immunoprecipitation followed by massive parallel DNA sequencing (ChIPseq) analysis of isolated adult murine cardiomyocytes from CamKII WT as well as from CaMKIIγ/CaMKIIδ double knockout (DKO) . DKO and WT cells were subjected to long-term Iso treatment for 24 h to maximize CaMKII-dependent H3S28p.

2019-06-13 | E-MTAB-8011 | biostudies-arrayexpress

Murine polyploid trophoblast giant cells from day E9.5 implantation sites

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

2013-04-30 | E-GEOD-45787 | biostudies-arrayexpress

ChIP-seq analysis of Gli1 and Sox2 input to neural progenitor program and integration with actve histone marks

Project description:In the vertebrate neural tube, regional Sonic hedgehog (Shh) signaling invokes a time- and concentration-dependent induction of six different cell populations mediated through Gli transcriptional regulators. Elsewhere in the embryo, Shh/Gli responses invoke different tissue appropriate regulatory programs. To elucidate Shh/Gli regulation of neural fate sepcification, we performed Gli1 ChIP-Seq analysis. We further analyzed two transcription factors whose motifs were enriched in Gli1 ChIP data (Sox2 and Foxa2). Two active histone marks (H3K4me2 and H3K27ac) were additionally analyzed to study activity status of Shh-responsive cis-elements. Active enhancer histone marks and transcription factor binding patterns were obtained from neuralized emrbyoid bodies. Biological replicates were performed for Gli1 and mock FLAG chips. Histone profiling for enhancer marks were taken from time course experiment performed in parallel.

2012-12-15 | E-GEOD-42132 | biostudies-arrayexpress

Chromatin immunoprecipitation of Drosophila to identify muscle differentiation factor Mef2 protein binding during embryonic development

Project description:Genomewide mapping of D. melanogaster the muscle differentiation factor Mef2 protein binding during embryonic development. Five consecutive timepoints (2-4, 4-6, 6-8, 8-10, 10-12 hrs after egg-laying) were assayed in two independent repeats each. Two different antibodies were used to precipitate the Mef2 protein. Additionally the respective preimmune-serum was used as a control for every precipitation. The enriched DNA was hybridized to high density Affymetrix GeneChip Drosophila Tiling 1.0R array.

2009-11-09 | E-TABM-649 | biostudies-arrayexpress

ChIP-seq data of Epstein-Barr Virus Nuclear Antigen Leader ProteinM-BM- (EBNALP)

Project description:Epstein-Barr-Virus (EBV) Nuclear Antigens EBNALP and EBNA2 are co-expressed in EBV infected B-lymphocytes and are critical for Lymphoblastoid Cell Line (LCL) growth. EBNALP removes NCOR1 and RBPJ repressive complexes from promoter and enhancer sites and EBNA2 mostly activates transcription from distal enhancers. ChIP-seqs found EBNALP at 19,224 LCL sites, which were 33% promoter associated. EBNALP was associated with 10 transcription factor (TF) clusters that included YY1(63%), SP1(62%), PAX5(59%), BATF(50%), IRF4(49%), RBPJ(43%), ETS1(39%), PU.1(37%), RAD21(33%), NF-kB(31%), TBLR1(26%), ZNF143(24%), CTCF(23%), SMC3(21%), and EBF(17%). EBNALP sites had higher H3K4me3, H3K9ac, H3K27ac, H2Az, and RNA Pol II signals than EBNA2 sites and had similar transcription effects. EBNALP co-localized with 29% of 19,845 EBNA2 sites. EBNALP/EBNA2 sites were similar to EBNALP sites in promoter localization, associated cell TFs, Pol II, H3K4me3, H3K9ac, H3K27ac, and H2Az signals. EBNALP and EBNA2 promoter sites were more transcriptionally active than EBNALP or EBNA2 promoter sites. EBNALP was at the enhancer or promoter of myc and MYC affected genes, including cyclin D2, and bcl2. EBNALP at promoters with DNA looping and transcription factors, is positioned to deplete repressors from enhancers and promoters, enable chromatin remodeling, and transcription activation. Two EBNALP ChIP-seq replicates from IB4 LCL are analyzed in this study.

2013-07-31 | E-GEOD-49338 | biostudies-arrayexpress

MEF2A Interactome in rat cardiomyocyte

Project description:Myocyte enhancer factor 2 A was immunoprecipitated from primary cardiomyocytes then sequenced along with its binding partners by LC-MS2 with data dependent acquisition and simultaneous isobaric label based quantification.

2023-02-21 | PXD038574 | Pride

Long-range chromosome interactions mediated by cohesin shape circadian gene expression [ChIP-Seq]

Project description:Mammalian circadian rhythm is established by the negative feedback loops consisting of a set of clock genes, which lead to the circadian expression of thousands of downstream genes. As genome-wide transcription is organized under the high-order chromosome structure, it is unclear how circadian gene expression is influenced by chromosome structure. In this study, we focus on the function of chromatin structure proteins cohesin as well as CTCF (CCCTC-binding factor) in circadian rhythm. We analyzed the interactome of a Bmal1-bound enhancer upstream of a clock gene, Nr1d1, by 4C-seq and observed that cohesin binding sites are enriched in the interactome. Integrating circadian transcriptome data and cistrome data, we found that cohesin-CTCF co-binding sites tend to insulate the phases of circadian oscillating genes while cohesin-non-CTCF sites facilitate the interaction between circadian enhancer and promoter. A coarse-grained model integrating the long-range effect of cohesin and CTCF markedly improved our mechanistic understanding of circadian gene expression. This model is subsequently supported by our RNA-seq data from cohesin knockout cells. Cohesin is required at least in part for driving the circadian gene expression by facilitating the enhancer-promoter looping. Taken together, our study provided a novel insight into the relationship between circadian transcriptome and the high-order chromosome structure. Bmal1 ChIP-Seq in WT mouse embryonic fibroblast cells

2016-04-04 | E-GEOD-77162 | biostudies-arrayexpress

VL30 retro-transposons are TRIM24-repressed enhancers that generate non-coding RNA to regulate gene expression in mouse hepatocytes. [ChIP-Seq]

Project description:TRIM24 and TRIM33 interact to form a corepressor complex that suppresses murine hepatocellular carcinoma (HCC). TRIM24 and TRIM33 cooperatively repress retinoic acid receptor dependent activity of VL30 retro-transposons in hepatocytes in vivo. In TRIM24 knockout hepatocytes, VL30 long terminal repeats (LTRs) generate enhancer (e)RNAs and act as surrogate promoter and enhancer elements deregulating expression of neighbouring genes. We show that a VL30 LTR-derived eRNA is essential to activate the lipocalin 13 gene in hepatocytes in vivo. A further consequence of VL30 de-repression is the accumulation of retro-transcribed VL30 DNA in the cytoplasm of TRIM24-mutant hepatocytes and activation of the viral defence/interferon response. VL30 activation therefore modulates gene expression via the enhancer activity of the LTRs and by activation of the interferon response. Both of these processes are genetically linked to HCC development suggesting that VL30 repression by TRIM24 plays an important role in tumour suppression. Examination of H3k4me3 and RNA pol II in liver by deep sequencing.

2013-01-01 | E-GEOD-39852 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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