Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

36 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ChIP-Seq for ERK2/MAPK1 and ELK1 in human embryonic stem cells

ABSTRACT: The ERK/MAPK signal transduction cascade is one of the key pathways regulating proliferation and differentiation in development and disease. In human embryonic stem cells (hESCs), ERK signaling is required for their self-renewing property. Here we studied the convergence of the ERK signaling cascade at the DNA by mapping genome-wide kinase-chromatin interactions for ERK2 in hESCs. We observe that ERK2 targets genes coding for small RNAs, histones, and genes involved in cellular metabolism and cell cycle. We find that the transcription factor ELK1 is essential in hESCs and that ERK2 co-occupies promoters bound by ELK1. Strikingly, promoters bound by ELK1 without ERK2 are occupied by Polycomb group proteins that repress genes involved in lineage commitment. In summary, we propose a model where extracellular signaling-stimulated proliferation and intrinsic repression of differentiation is integrated to maintain the identity of hESCs.

INSTRUMENT(S): Illumina Genome Analyzer II

ORGANISM(S): Homo sapiens

SUBMITTER: Jonathan Goke

PROVIDER: E-MTAB-1565 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Transcriptional profiling by array after knockdown of ERK2 and ELK1 in human embryonic stem cells

Project description:The ERK/MAPK signal transduction cascade is one of the key pathways regulating proliferation and differentiation in development and disease. In human embryonic stem cells (hESCs), ERK signaling is required for their self-renewing property. Here we studied the convergence of the ERK signaling cascade at the DNA by mapping genome-wide kinase-chromatin interactions for ERK2 in hESCs. We observe that ERK2 targets genes coding for small RNAs, histones, and genes involved in cellular metabolism and cell cycle. We find that the transcription factor ELK1 is essential in hESCs and that ERK2 co-occupies promoters bound by ELK1. Strikingly, promoters bound by ELK1 without ERK2 are occupied by Polycomb group proteins that repress genes involved in lineage commitment. In summary, we propose a model where extracellular signaling-stimulated proliferation and intrinsic repression of differentiation is integrated to maintain the identity of hESCs.

2013-05-31 | E-MTAB-1583 | biostudies-arrayexpress

ChIP-Seq of Histone Modifications in 3iL Human Embryonic Stem Cells

Project description:Human embryonic stem cells (hESCs) are isolated from the inner cell mass of the blastocysts. The pluripotent properties of hESCs enable the derivation of cell-types or tissues of different lineages for potential applications such as therapeutics discovery and regenerative medicine. Even though hESCs are pluripotent, differences have been observed when compared to the native pluripotent epiblast cells of the blastocyst. We use a chemical approach (3iL: 3 small molecule inhibitor and cytokine) to induce an expression signature that more closely resembles native pluripotent cells. This experiment is the epigenetic data of the study.

2013-12-05 | E-MTAB-2041 | biostudies-arrayexpress

ChIP-seq of H1 human embryonic stem cells (hESCs) to map the global binding profile of EZH2 to investigate the association of PRDM14 binding with the PRC2 in hESCs

Project description:An experiment was performed to map the global binding profile of EZH2 in human embryonic stem cells (hESCs). How the Polycomb Repressive Complex 2 (PRC2) is recruited to the DNA in hESC remains largely unknown. Previous studies on the transcription factor PRDM14 suggested that PRDM14 plays a repressive role in hESCs. Here, we mapped the global binding profile of EZH2 in hESC to investigate the association of PRDM14 binding with the PRC2 in hESCs. EZH2 binding is found to be enriched in PRDM14 binding sites. The PRC2 dependent repressive role of PRDM14 is further supported by the strong correlation of PRDM14 binding with the repressive histone modification H3K27me3.

2012-11-01 | E-MTAB-1305 | biostudies-arrayexpress

ChIP-Seq of OCT4, NANOG, p300 in 3iL Human Embryonic Stem Cells

2013-12-05 | E-MTAB-2044 | biostudies-arrayexpress

ChIP-Seq of STAT3 in 3iL Human Embryonic Stem Cells

2013-12-05 | E-MTAB-2042 | biostudies-arrayexpress

PHB Acts as a Member of the HIRA Complex to Control an Epigenetic and Metabolic Circuitry

Project description:Cellular metabolism and chromatin landscape both contribute to cell fate determination. However, their interplay remains poorly understood. Here we show that Prohibitin (PHB), an evolutionarily conserved protein, involves in a histone variant H3.3 chaperon HIRA complex-dependent epigenetic and metabolic circuitry to maintain the identity of human embryonic stem cells (hESCs). We found that silencing of PHB triggers hESC differentiation with concomitant enhancements of histone 3 (H3) lysine (K) methyl modifications as a result of the reduced production of Î±-ketoglutarate (Î±-KG), a metabolite required for activities of many dioxygenase and in turn chromatin structure1,2. Mechanistically, PHB acts as a functional member of the HIRA complex3,4. Resembling PHB deficiency, loss of HIRA in hESCs leads to massive differentiation and aberrant histone modifications, although it was previously found not to disrupt the self-renewal in mouse ESCs (mESCs)5. Genome-wide H3.3 ChIP- sequence analyses indicate that reduction of H3.3 deposition caused by PHB knock down is extremely similar to that induced by HIRA knock down. Specifically, silencing either HIRA or PHB leads to repressive chromatin characters at promoters of pluripotency genes and isocitrate dehydrogenases (IDHs), the enzyme responsible for Î±-KG production, but active chromatin features at promoters of developmental genes, paralleling to transcript levels of these genes. Our results identify PHB as an essential factor not only for hESC self-renewal but also for the proper function of the HIRA complex, linking the HIRA complex-dependent H3.3 deposition to the production of a critical metabolite required for shaping chromatin structure, and demonstrating the importance of the interplay between epigenetic state and metabolic regulation in cell fate determination. Examination of H3.3 deposition in NT, PHB, and HIRA siRNA treated hESCs respectively.

2016-08-11 | E-GEOD-72143 | biostudies-arrayexpress

ChIP-seq of Klf2 in mouse embryonic stem cells (Serum/LIF and 2i)

Project description:The self-renewing pluripotent state was first captured in mouse embryonic stem cells (mESCs) over two decades ago. The standard condition requires the presence of serum and LIF, which provide growth promoting signals for cell expansion. However, there are pro-differentiation signals which destabilize the undifferentiated state of mESCs. The dual inhibition (2i) of the pro-differentiation Mek/Erk and Gsk3/Tcf3 pathways in mESCs is sufficient to establish an enhanced pluripotent “ground state” which bears features resembling the pre-implantation mouse epiblast. Gsk3 inhibition alleviates the repression of Esrrb, a transcription factor that can substitute for Nanog function in mESCs. The molecular mechanism that is mediated by Mek inhibition is however not clear. In this study, we investigate the pathway through which Mek inhibition operates to maintain ground state pluripotency. We have found that in mESCs, Kruppel-like factor 2 (Klf2) is a protein target of the Mek/Erk pathway; and that Klf2 protein is phosphorylated by Erk2 and subsequently degraded through the proteosome. It is therefore by Mek-inhibition through PD0325901 or 2i that enables the stabilization and accumulation of Klf2 to sustain ground state pluripotency. Importantly, we found that Klf2-null mESCs, while viable under LIF/Serum conditions, cannot be maintained and eventually gradually die within a few passages. Our result thus demonstrates that Klf2 is an essential factor of ground state pluripotency. Collectively, our study defines the Mek/Klf2 axis that cooperates with the Gsk3/Esrrb pathway in mediating ground state pluripotency.

2014-06-04 | E-MTAB-2365 | biostudies-arrayexpress

Proteomic investigation of the effect of DAP5 knock-down on human embryonic stem cells

Project description:We performed a deep mass-spec analysis to determine DAP5 proteomic signature on human embryonic stem cells (hESCs) by evaluating the steady state proteins level on DAP5-KD and NT control cells.

2022-08-10 | PXD030717 | Pride

RNA-seq of canine MDCK epithelial cell line compared to cell line overexpressing ERK2 or cell line with conditional activation of the ERK pathway

Project description:Using RNA-seq and canine MDCK epithelial cells, we analyzed mRNA expression profiles of cells overexpressing ERK2 and cells where the ERK pathway was activated for 24 hrs. For this purpose, three cell lines were used: parental MDCK cells, MDCK cells overexpressing FLAG-ERK2 or MDCK cells expressing conditionally active Raf protein (ΔRaf1:ER). Activation of the ERK pathways was achieved by the addition of 4-Hydroxytamoxifen that converts ΔRaf1:ER protein to the active form and it subsequently activates the ERK pathway.

2022-10-01 | E-MTAB-12132 | biostudies-arrayexpress

ChIP-seq of definitive endoderm differentiation of human embryonic stem cells in early G1 phase of the cell cycle

Project description:The experiment was designed to investigate histone modification changes during cell cycle progression of human embryonic stem cells (hESCs) during definitive endoderm differentiation. For this, FUCCI hESCs were sorted in Early G1 (EG1), and differentiation into endoderm was performed for up to 72 hours with a combination of cytokines as described in Pauklin and Vallier (2013) and Pauklin et al. (2016). ChIP-seq was generated at 12-hour and 36-hour time-points for H3K4me3, H3K27ac, H3K4me1, H3K36me3 and H3K27me3. Library preparation and sequencing were performed at the Wellcome Sanger Institute next-generation sequencing facility on Illumina HiSeq 2000, 2 x 75bp paired-end reads. ChIP-seq data from other time-points (0h, 24h, 48h and 72h) of the same experimental set-up is available elsewhere (GEO DataSet, accession PRJNA593217). All processed ChIP-seq data is publicly available at http://ngs.sanger.ac.uk/production/endoderm

2020-09-07 | E-MTAB-9276 | 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