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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Trim24 knock down in the 2i-state of the mouse ES cells

ABSTRACT: Differentially expressed genes were determined by single-end sequencing (stranded protocol) following Trim24 and/or p53 knock down in the mouse ES cells grown in 2i media. Triplicates were generated for treatment and control samples but for p53 knock down (duplicate).

ORGANISM(S): Mus musculus

SUBMITTER: Charles Girardot

PROVIDER: E-MTAB-4893 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Expanding the Circuitry of Pluripotency by Selective Isolation of Chromatin-Associated Proteins.

Rafiee Mahmoud-Reza MR Girardot Charles C Sigismondo Gianluca G Krijgsveld Jeroen J

Molecular cell 20161020 3

Maintenance of pluripotency is regulated by a network of transcription factors coordinated by Oct4, Sox2, and Nanog (OSN), yet a systematic investigation of the composition and dynamics of the OSN protein network specifically on chromatin is still missing. Here we have developed a method combining ChIP with selective isolation of chromatin-associated proteins (SICAP) followed by mass spectrometry to identify chromatin-bound partners of a protein of interest. ChIP-SICAP in mouse embryonic stem ce ...[more]

PMID: 27773674

Similar Datasets

Trim24 ChIP-seq in embryonic stem (ES) cells grown by 2i+LIF (2iL) and serum media

Project description:ChIP followed by next generation sequencing against Trim24 was performed in mouse embryonic stem (ES) grown either in 2i+LIF (2iL) or serum media. Two biological replicates for each condition were sequenced using Illumina HiSeq. Two input controls (no IP) were also generated for each condition.

2016-11-08 | E-MTAB-3802 | biostudies-arrayexpress

Dzip3 regulates developmental genes in mouse embryonic stem cells by reorganizing 3D chromatin conformation [RNA-seq]

Project description:In mouse embryonic stem cells (mES cells), ubiquitylation of histone H2A lysine 119 represses a large number of developmental genes and maintains mES cell pluripotency. It has been suggested that a number of H2A ubiquitin ligases as well as deubiquitylases and related peptide fragments contribute to a delicate balance between self-renewal and multi-lineage differentiation in mES cells. Here, we tested whether known H2A ubiquitin ligases and deubiquitylases are involved in mES cell regulation and discovered that Dzip3, the E3 ligase of H2AK119, represses differentiation-inducible genes as well as Ring1B. The two sets of target genes partially overlapped but had different spectra. We found that Dzip3 represses gene expression by orchestrating changes in 3D organization in addition to regulating ubiquitylation of H2A. Our results shed light on the epigenetic mechanism of transcriptional regulation, which depends on 3D chromatin reorganization to regulate mES cell differentiation. mouse ES cell mRNA profiles of control, Ring1B knock down, and Dzip3 knock down, in duplicate, using Illumina MiSeq.

2015-12-08 | E-GEOD-71882 | biostudies-arrayexpress

Expression data of hiPSC-derived anterior foregut endoderm cells (AFECs), ventral anterior foregut cells (VAFECs), EpCAM+CPM+ and EpCAM+CPM- cells and CPM+ cells sorted from VAFECs

Project description:Specific surface marker for NKX2-1+ VAFECs may be helpful for isolating a homogeneous population of alveolar epithelial progenitor cells and distinguishing the differentiation from a thyroid lineage to a lung lineage. In order to identify specific markers of VAFECs, a microarray analysis was performed to compare the global gene expression patterns between AFECs and VAFECs in 201B7 hiPSCs. We hypothesized that NKX2-1+ cells could be purified by sorting CPM+ VAFECs. After dissociating VAFECs cells on day 14 with Accutase, FACS was performed using anti-EPCAM and anti-CPM antibodies. EPCAM+CPM+ and EPCAM+CPM- cells were then sorted, and the global gene expression patterns of these two populations were examined using a microarray analysis. In addition, MACS was performed to obtain CPM+ cells for comparison. We extracted total RNA from hiPSCs-derived AFECs, VAFECs, EPCAM+CPM+ and EPCAM+CPM- VAFECs and CPM+ VAFECs and hybridized them to Affymetrix microarrays.

2014-08-25 | E-GEOD-53513 | biostudies-arrayexpress

Using ribosome profiling to investigate the effect of p53 on translation in cancer cells

Project description:p53 is deleted or dysfunctional, or develops these features during the course of disease, with a frequency of about 50% in human cancers. This is clinically important because this group of patients respond very poorly to treatment. Our approach to discovering novel biomarkers or targets for therapy for p53 deleted/dysfunctional disease is to find genes that are translationally regulated by p53. The aim of this experiment is to compare translational efficiencies in cancer cells that are p53 WT, p53-/-, or p53 R175H, in response to doxorubicin.

2021-02-22 | E-MTAB-8100 | biostudies-arrayexpress

Xist exploits three-dimensional chromosome architecture to spread across the X-chromosome

Project description:Many large noncoding RNAs (lncRNAs) regulate chromatin, but the mechanisms by which they localize to genomic targets remain unexplored. Here we investigate the localization mechanisms of Xist during X-chromosome inactivation (XCI), a paradigm of lncRNA-mediated chromatin regulation. During the maintenance of XCI, Xist binds broadly across the X-chromosome. During initiation of XCI, Xist initially transfers to distal regions across the X-chromosome that are not defined by specific sequences. Instead, Xist identifies these regions by exploiting the three-dimensional conformation of the X-chromosome. Xist initially accumulates on the periphery of actively transcribed regions and requires its silencing domain to spread across active regions. This suggests a model where Xist coats the entire X-chromosome by searching in three dimensions, modifying chromosome structure, and spreading to newly accessible locations. We examined the genomic localization of the Xist lncRNA using RNA Antisense Purification (RAP) in multiple cell contexts: 1) differentiated female cells (MLFs); 2) a time-course of Xist localization in male embryonic stem (ES) cells where the endogenous Xist promoter is replaced by a tet-inducible one (pSM33); 3) a time-course of Xist localization in differentiating female ES cells (F1 2-1); and 4) wild-type (delXF6) and A-repeat deletion (delSXC9) Xist transgenes incorporated into the Hprt locus under the control of a tet-inducible promoter.

2013-05-30 | E-GEOD-46918 | biostudies-arrayexpress

p53-regulated networks of protein, mRNA, miRNA and lncRNA expression revealed by integrated pSILAC and NGS analyses

Project description:We determined the effect of p53 activation on de novo protein synthesis using quantitative proteomics of newly synthesized proteins (pulsed stable isotope labeling with amino acids in cell culture, pSILAC) in combination with mRNA and non-coding RNA expression analyses by next generation sequencing (RNA-, miR-Seq) in the colorectal cancer (CRC) cell line SW480. Furthermore, genome-wide DNA binding of p53 was analyzed by chromatin-immunoprecipitation (ChIP-Seq). Thereby, we identified differentially regulated mRNAs (1258 up, 415 down), miRNAs (111 up, 95 down), lncRNAs (270 up, 123 down) and proteins (542 up, 569 down). Changes in mRNA and protein expression levels showed a positive correlation (r = 0.50, p < 0.0001). More transcriptionally induced genes displayed occupied p53 binding sites (4.3% mRNAs, 7.2% miRNAs, 6.3% lncRNAs, 5.9% proteins) than repressed genes (2.4% mRNAs, 3.2% miRNAs, 0.8% lncRNAs, 1.9% proteins), suggesting indirect mechanisms of repression. Around 50% of the downregulated proteins displayed seed-matching sequences of p53-induced miRNAs in the corresponding 3’-UTRs. Moreover, proteins repressed by p53 significantly overlapped with those previously shown to be repressed by miR-34a. We confirmed upregulation of the novel direct p53 target genes LINC01021, MDFI, ST14 and miR-486 and showed that ectopic LINC01021 expression inhibited proliferation in SW480 cells. Furthermore, HMGB1, KLF12 and CIT mRNAs were confirmed as direct targets of the p53-induced miR-34a, miR-205 and miR-486-5p, respectively. In line with the loss of p53 function during tumor progression, elevated expression of HMGB1, KLF12 and CIT was detected in advanced stages of cancer. This study provides new insights and a comprehensive catalogue of p53-mediated regulations and p53 DNA binding in CRC cells.

2015-07-23 | PXD001976 | Pride

Expression data from mouse embryo fibroblast (MEFS)

Project description:The role of p53 in assuring longevity through prevention of cancer is well established, but how it specifically regulates aging is still controversial. Our assumption is that distinct p53-pathways regulate tumor suppression and aging and that p66Shc is one of the master regulators of the p53 aging function. p66Shc longevity determinant protein acts as a downstream target of p53 and it is indispensable for the ability of activated p53 to induce elevation of intracellular oxidants and apoptosis. We used microarray to gain insight into the mechanism through which p66Shc could regulate p53 oxidative stress dependent activity. Total RNA was extracted from Primary murine embryonic fibroblasts (MEFs) were isolated from 13.5-day-old embryos according to standard procedures from WT, p53KO and p66ShcKO mice. Treatment: Early passage (p.2) MEFs were washed twice with PBS1X solution, and then incubated in DMEM media containing 400 Î¼M of H2O2 or 0.25Î¼g/ml of Doxorubicin (SIGMA) at 37Â°C for four hours.

2012-04-01 | E-GEOD-28416 | biostudies-arrayexpress

TETs controls maintenance DNA methylation via the regulation of Dppa3

Project description:Dissection of catalytic and non-catalytic functions of Tet1 and Tet2. Transcriptome profiling of wild type, Tet1 catalytic mutants, Tet2 and Tet1/2 catalytic mutant catalytic during EpiLC differentiation.

2020-10-05 | E-MTAB-6797 | biostudies-arrayexpress

Transcription profiling of human NIH 3T3 inducible cell line to study the role of PKR in regulating gene expression

Project description:PKR is an interferon induced serine/threonine protein kinase, that is activated by double stranded RNA. PKR plays an important role in the antiviral defense by interferon. In addition to its role in translation, PKR participates in several signaling pathways to transcription. The goal of this experiment is to study the role of PKR in regulating gene expression in our NIH 3T3 inducible cell line, which could overexpress PKR wt protein after the removal of tetracycline (Donze O, Dostie J, Sonenberg N. (1999) Virology 256: 322-9).

2004-01-30 | E-MEXP-50 | biostudies-arrayexpress

Mutant p53R273H regulated microRNA profiling in presence and absence of DNA damage in H1299 cells

Project description:In the present study, we used a high-throughput small RNA deep sequencing followed by a systematic computational analysis to identify genome wide mutant p53R273H regulated miRNAs in both DNA damage dependent and independent context. Several miRNA-mRNA regulatory networks have been predicted that might contribute to mutant p53 GOF properties. Differentially regulated miRNA signature profile has been validated in the lung cancer patients harboring wildtype and mutant p53. We identified specific miRNA signatures for lymph node metastasis associated with p53 mutation in lung adenocarcinoma and also predicted the possible contribution of two mutant p53 regulated miRNAs in EMT process. Furthermore, this study identified a hitherto unknown miRNA in human which might act as one of the crucial downstream targets of GOF mutant p53 to confer oncogenic properties. Determination of mutant p53R273H regulated microRNAs H1299 cells.

2017-04-28 | E-GEOD-68353 | biostudies-arrayexpress

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