Mus musculus
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ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE65491
PROVIDER: PRJNA142241 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE26360: Genome-wide analysis revealed a crosstalk between p53 and the pluripotent gene networks in mouse embryonic stem cells (expression) GSE26361: Genome-wide analysis revealed a crosstalk between p53 and the pluripotent gene networks in mouse embryonic stem cells (ChIP-Seq) Refer to individual Series
2012-03-05 | E-GEOD-26362 | biostudies-arrayexpress
Project description:Genome-wide analysis revealed a crosstalk between p53 and the pluripotent gene networks in mouse embryonic stem cells (expression)
| PRJNA142239 | ENA
Project description:The tumor suppressor p53 regulates the differentiation of embryonic stem (ES) cells upon DNA damage. However, our understanding of this critical tumor suppressive role of p53 in ES cells is limited, mainly because of the lack of molecular mechanism. Here, we report a widespread cross-regulation of p53-mediated DNA damage signaling and the pluripotent gene network in ES cells using chromatin-immunoprecipitation assay-based sequencing (ChIP-seq) and gene expression microarray. Upon DNA damage, p53 directly regulates the transcription of 3644 genes (p<0.005) in mouse ES cells. Genome-wide analysis revealed a dramatic difference between the regulation of p53-activated and -repressed genes. p53 mainly regulates the promoter regions of activated genes, whereas the main regulatory regions for repressed genes reside in distal regions. Among p53-repressed genes, many are pluripotent transcription factors of ES cells, such as Oct4, Nanog, Sox2, Esrrb, c-Myc, n-Myc and Sall4. Strikingly, these transcriptional factors also directly regulate the transcription of the Trp53 gene, highlighting a previously under-estimated transcriptional regulation of p53 in ES cells. Therefore, p53 signaling and ES pluripotent transcriptional networks form an intertwined circuitry. Together, our results provide mechanistic insights into the crosstalk of p53-mediated DNA damage and ES cell "stemness" transcriptional gene networks and shed light on the tumor suppressive function of p53 in ES cells. The goal of this experiment is to identify the gene expression changes after adriamycin treatment in a p53-dependent manner. Total six samples: triplicates for untreated mES cells and triplicates for mES cells treated with adriamycin.
2012-03-05 | E-GEOD-26360 | biostudies-arrayexpress
Project description:Chavez2009 - a core regulatory network of OCT4 in human embryonic stem cells
A core OCT4-regulated network has been identified as a test case, to analyase stem cell characteristics and cellular differentiation.
This model is described in the article:
In silico identification of a core regulatory network of OCT4 in human embryonic stem cells using an integrated approach.
Chavez L, Bais AS, Vingron M, Lehrach H, Adjaye J, Herwig R
BMC Genomics, 2009, 10:314
Abstract:
BACKGROUND: The transcription factor OCT4 is highly expressed in pluripotent embryonic stem cells which are derived from the inner cell mass of mammalian blastocysts. Pluripotency and self renewal are controlled by a transcription regulatory network governed by the transcription factors OCT4, SOX2 and NANOG. Recent studies on reprogramming somatic cells to induced pluripotent stem cells highlight OCT4 as a key regulator of pluripotency.
RESULTS: We have carried out an integrated analysis of high-throughput data (ChIP-on-chip and RNAi experiments along with promoter sequence analysis of putative target genes) and identified a core OCT4 regulatory network in human embryonic stem cells consisting of 33 target genes. Enrichment analysis with these target genes revealed that this integrative analysis increases the functional information content by factors of 1.3 - 4.7 compared to the individual studies. In order to identify potential regulatory co-factors of OCT4, we performed a de novo motif analysis. In addition to known validated OCT4 motifs we obtained binding sites similar to motifs recognized by further regulators of pluripotency and development; e.g. the heterodimer of the transcription factors C-MYC and MAX, a prerequisite for C-MYC transcriptional activity that leads to cell growth and proliferation.
CONCLUSION: Our analysis shows how heterogeneous functional information can be integrated in order to reconstruct gene regulatory networks. As a test case we identified a core OCT4-regulated network that is important for the analysis of stem cell characteristics and cellular differentiation. Functional information is largely enriched using different experimental results. The de novo motif discovery identified well-known regulators closely connected to the OCT4 network as well as potential new regulators of pluripotency and differentiation. These results provide the basis for further targeted functional studies.
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2005-01-01 | MODEL1305010000 | BioModels
Project description:The tumor suppressor p53 regulates the differentiation of embryonic stem (ES) cells upon DNA damage. However, our understanding of this critical tumor suppressive role of p53 in ES cells is limited, mainly because of the lack of molecular mechanism. Here, we report a widespread cross-regulation of p53-mediated DNA damage signaling and the pluripotent gene network in ES cells using chromatin-immunoprecipitation assay-based sequencing (ChIP-seq) and gene expression microarray. Upon DNA damage, p53 directly regulates the transcription of 3644 genes (p<0.005) in mouse ES cells. Genome-wide analysis revealed a dramatic difference between the regulation of p53-activated and -repressed genes. p53 mainly regulates the promoter regions of activated genes, whereas the main regulatory regions for repressed genes reside in distal regions. Among p53-repressed genes, many are pluripotent transcription factors of ES cells, such as Oct4, Nanog, Sox2, Esrrb, c-Myc, n-Myc and Sall4. Strikingly, these transcriptional factors also directly regulate the transcription of the Trp53 gene, highlighting a previously under-estimated transcriptional regulation of p53 in ES cells. Therefore, p53 signaling and ES pluripotent transcriptional networks form an intertwined circuitry. Together, our results provide mechanistic insights into the crosstalk of p53-mediated DNA damage and ES cell "stemness" transcriptional gene networks and shed light on the tumor suppressive function of p53 in ES cells.
2012-03-05 | GSE26360 | GEO
Project description:mouse embryonic fibroblasts, embryonic stem cells, and induced pluripotent stem cells were compared via metabolomic analysis
2018-08-02 | MSV000082680 | GNPS
Project description:Pluripotency is highly dynamic and progresses through a continuum of pluripotent stem-cell states. The two states that bookend the pluripotency continuum, naïve and primed, are well characterized, but our understanding of the intermediate states and transitions between them remain incomplete. Here, we dissect the dynamics of pluripotent state transitions underlying pre- to post-implantation epiblast differentiation. Through comprehensive mapping of the proteome, phosphoproteome, transcriptome, and epigenome of embryonic stem cells transitioning from naïve to primed pluripotency, we find that rapid, acute, and widespread changes to the phosphoproteome precede ordered changes to the epigenome, transcriptome, and proteome. Reconstruction of kinase-substrate networks reveals signaling cascades, dynamics, and crosstalk. Distinct waves of global proteomic changes mark discrete phases of pluripotency, with cell state-specific surface markers tracking pluripotent state transitions. Our data provide new insights into the multi-layered control of the phased progression of pluripotency and a foundation for modeling mechanisms regulating pluripotent state transitions (www.stemcellatlasorg).
2019-05-07 | PXD010621 | Pride
Project description:mouse embryonic fibroblasts, embryonic stem cells, and induced pluripotent stem cells were compared via metabolomic analysis
2013-01-16 | ST000003 | MetabolomicsWorkbench
Project description:Many transcriptional and epigenetic networks must be integrated to maintain self-renewal and pluripotency in embryonic stem cells (ESCs) and to enable induced pluripotent stem cell (iPSC) reprogramming. Here, we explore the role of Zfp217 as a key transcriptional factor in maintaining ES cell self-renewal by permorming genome-wide ChIP-Seq analyses. Examination of Zfp217 binding profiling by high throughput sequencing in mouse stem cells
2015-10-30 | E-GEOD-65730 | biostudies-arrayexpress
Project description:Many transcriptional and epigenetic networks must be integrated to maintain self-renewal and pluripotency in embryonic stem cells (ESCs) and to enable induced pluripotent stem cell (iPSC) reprogramming. Here, we explore the role of Zfp217 as a key transcriptional factor in maintaining ES cell self-renewal by permorming genome-wide ChIP-Seq analyses.
2015-10-30 | GSE65730 | GEO