Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA361220 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5172111_1.fastq.gz | Fastqsanger.gz | |||
| SRR5172111_2.fastq.gz | Fastqsanger.gz | |||
| SRR5172112_1.fastq.gz | Fastqsanger.gz | |||
| SRR5172112_2.fastq.gz | Fastqsanger.gz | |||
| SRR5172113_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
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Project description:Among its many roles in development, retinoic acid determines the anterior-posterior identity of differentiating motor neurons by activating Retinoic Acid Receptor (RAR)-mediated transcription. RAR is thought to bind the genome constitutively, and only induce transcription in the presence of the retinoid ligand. However, little is known about where RAR binds to the genome or how it selects target sites. We tested the constitutive RAR binding model using the retinoic acid-driven differentiation of mouse embryonic stem cells into differentiated motor neurons. We find that retinoic acid treatment results in widespread changes in RAR genomic binding, including novel binding to genes directly responsible for anterior-posterior specification, as well as the subsequent recruitment of the basal polymerase machinery. Finally, we discovered that the binding of transcription factors at the embryonic stem cell stage can accurately predict where in the genome RAR binds after initial differentiation. We have characterized a ligand-dependent shift in RAR genomic occupancy at the initiation of neurogenesis. Our data also suggests that enhancers active in pluripotent embryonic stem cells may be preselecting regions that will be activated by RAR during neuronal differentiation. The differentiation of ventral motor neurons is induced by treating embryonic stem cell cultures with retinoic acid. Here, ChIP-seq is used to profile the genome-wide occupancy of RAR isofroms both immediately prior to and during exposure of the cells to retinoic acid. ChIP-seq is also used to profile the genomic occupancy of Pol2 with phosphorylated serine 5 (Pol2-S5P) and phosphorylated serine 2 (Pol2-S2P) after exposure to retinoic acid.
2010-12-10 | E-GEOD-19409 | biostudies-arrayexpress
Project description:miRNAs are involved in stem cell differentiation and we wanted to investigate miRNAs involved in embryonic stem cell differentiation towards renal lineage. Mouse embryonic stem cells were cultured with a renal differentiation medium (suplemented with All-trans-retinoic acid and Activin A) or in a control media, in orther to determine the miRNAs variations between these groups.
2013-02-22 | E-MTAB-1468 | biostudies-arrayexpress
Project description:All-trans retinoic acid (ATRA) alters gene expression in CCE WT embryonic stem cells, but has no effect on gene expression in RAR-deficient TKO cells (devoid of Retinoic Acid Receptors α, β, and γ)
2018-05-25 | GSE112412 | GEO
Project description:Expression profile of miRNAs during retinoic acid (RA) induced differentiation of mose embryonic stem cells Expression profile of mRNAs during retinoic acid (RA) amd miR-134 induced differentiation of mouse embryonic stem cells. Keywords: affymetrix custom array and illumina MouseRef-8
2006-03-24 | GSE4522 | GEO
Project description:Retinoic acid receptors (RARs) ?, ?, and ? heterodimerize with Retinoid X receptors (RXR) ?, ?, and ? and bind the cis-acting response elements known as RAREs to execute the biological functions of retinoic acid during mammalian development. RAR? mediates the anti-proliferative and apoptotic effects of retinoids in certain tissues and cancer cells, such as melanoma and neuroblastoma cells. Furthermore, ablation of RAR? enhanced the tumor incidence of Ras transformed keratinocytes and was associated with resistance to retinoid mediated growth arrest and apoptosis. We used microarray analysis to identify genes, which upon 8 or 24 hr of treatment with all-trans retinoic acid display differential expression in RAR? knockout (RAR?KO) murine embryonic stem cells relative to CCE WT cells. We demonstrate that following RA treatment the majority of inducible transcripts are present at lower levels in RAR?KO ES cells compared to WT ES cells. Murine embryonic stem cells (WT and RAR?KO) were treated with either all-trans retinoic acid (up to 24 hr) or with vehicle control (EtOH).
2012-12-31 | E-GEOD-43221 | biostudies-arrayexpress
Project description:Human neuronal differentiation alters responsiveness to innate immune stimuli and virus infections. We used microarrays to examine the transcriptional responses of the human BE(2)-C neuroblastoma cell line to retinoic acid-induced differentiation and type I IFN stimulation. Experiment Overall Design: Cultured BE(2)-C cells were differentiated with 10 uM all-trans retinoic acid (RA) for 3 weeks, incubated with universal type I IFN (IFNa-A/D) for 6 or 12 h, and Affymetrix Human Genome Array U133 Plus 2.0 chips were used to analyze transcript levels.
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Project description:Among its many roles in development, retinoic acid determines the anterior-posterior identity of differentiating motor neurons by activating Retinoic Acid Receptor (RAR)-mediated transcription. RAR is thought to bind the genome constitutively, and only induce transcription in the presence of the retinoid ligand. However, little is known about where RAR binds to the genome or how it selects target sites. We tested the constitutive RAR binding model using the retinoic acid-driven differentiation of mouse embryonic stem cells into differentiated motor neurons. We find that retinoic acid treatment results in widespread changes in RAR genomic binding, including novel binding to genes directly responsible for anterior-posterior specification, as well as the subsequent recruitment of the basal polymerase machinery. Finally, we discovered that the binding of transcription factors at the embryonic stem cell stage can accurately predict where in the genome RAR binds after initial differentiation. We have characterized a ligand-dependent shift in RAR genomic occupancy at the initiation of neurogenesis. Our data also suggests that enhancers active in pluripotent embryonic stem cells may be preselecting regions that will be activated by RAR during neuronal differentiation.
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Project description:The main scientific objective of the project was to investigate whether Lamin A/C could be involved in neuroblastoma differentiation. Moreover, taking into account the significance of differentiation stage in the neuroblastoma tumor progression we have also studied a possible role of Lamin A/C in the tumorigenesis of this neuronal cancer. As differentiating stimulus we used the all-trans retinoic acid (RA), the most effective compound which has been shown to induce differentiation in neuroblastoma cells. To get insight into the impairment of cell differentiation produced by the LMNA (Lamin A/C) silencing in SHSY5Y cells, we compared the gene expression profile of control and silenced cells both in Retinoic Acid treated and untreated samples, using the one-color Agilent microarray platform. Four condition experiment: cells infected with a mock vector (Mock cells), treated and untreated with retinoic acid (RA); cells infected with a silencing vector for LMNA (LMNA-KD cells), treated and untreated with retinoic acid.
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Project description:Embryonic stem cells (ESC) are derived from blastocyst-stage embryos and are thought to be functionally equivalent to the inner cell mass in their developmental potential. ESCs pluripotency is maintained through a complex interplay of different signaling pathways and a network of transcription factors, which is centered around Oct3/4, Sox2 and Nanog. Although, in general, much is known about this pluripotency self-renewal circuitry, the molecular events that lead ESC to exit from pluripotency and begin differentiation are currently less known. Retinoic acid, an active metabolite of the vitamin A (retinol), plays important and pleiotropic roles in vertebrate embryonic development and ESC differentiation. Here we demonstrate that RA promotes early steps of ESC differentiation, and that ESC increase their capacity to synthesize RA during spontaneous differentiation as embryoid bodies, up-regulating the RA biosynthetic pathway components RDH1, RDH10, ADH3, RALDH2, and CRABP2. Microarray derived from total RNA of mESC not treated or treated with all-trans retinoic acid (ATRA) for 2 hours.
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