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accession-icon SRP055200
The Effects of Nanog HD Mutants on Mouse Embryonic Stem Cells
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We examined global gene expression patterns of mouse embryonic stem cells overexpressing EGFP, Nanog wild-type, or Nanog L122A mutants in normal, "-LIF" or "+RA" culture conditions by RNA-seq experiments. In “+RA” culture conditions, the expression patterns of the RA-responsive genes were slightly different in WT transfectants and more different in L122A transfectants compared with EGFP transfectants. These results suggested that L122A transfectants showed partial resistant activity against RA-induced differentiation, which was not found in WT mNANOG transfectants. Overall design: Examination of 3 different transfectants from mouse embryonic stem cell, RF8 line, in 3 different culture conditions.

Publication Title

Structure-based discovery of NANOG variant with enhanced properties to promote self-renewal and reprogramming of pluripotent stem cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP065040
A Primate lncRNA Mediates Notch Signaling During Neuronal Development by Sequestering miRNA [single cell sequencing analysis]
  • organism-icon Homo sapiens
  • sample-icon 240 Downloadable Samples
  • Technology Badge IconNextSeq500

Description

Long non-coding RNAs (lncRNAs) are a diverse category of transcripts with poor conservation and have expanded greatly in primates, particularly in their brain. We identified a lncRNA, which has acquired 16 microRNA response elements (MREs) for miR-143-3p in the Catarrhini branch of primates. This lncRNA termed LncND (neuro-development) gets expressed in neural progenitor cells and then declines in mature neurons. Binding and release of miR-143-3p, by LncND, can control the expression of Notch. Its expression is highest in radial glia cells in the ventricular and outer subventricular zones of human fetal brain. Down-regulation of LncND in neuroblastoma cells reduced cell proliferation and induced neuronal differentiation, an effect phenocopied by miR-143-3p over-expression and supported by RNA-seq analysis. These findings support a role for LncND in miRNA-mediated regulation of Notch signaling in the expansion of the neural progenitor pool of primates and hence contributing to the rapid growth of the cerebral cortex. Overall design: Cerebral organoids were generated as in Lancaster et al. (Lancaster and Knoblich, 2014). Organoids were dissociated into single cells and captured on C1 Single-Cell Auto Prep Integrated Fluidic Circuit (IFC) (Fluidigm). The RNA extraction and amplification was performed on the chip as described by the manufacturer. We captured 68 single-cells on a C1 Single-Cell Auto Prep System (Fluidigm) and sequenced the RNA on a NextSeq500 System (Illumina) (Pollen et al., 2014). Out of 68 cells, we obtained 60 high quality cells.

Publication Title

A Primate lncRNA Mediates Notch Signaling during Neuronal Development by Sequestering miRNA.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP064761
A Primate lncRNA Mediates Notch Signaling During Neuronal Development by Sequestering miRNA [SHSY5Y cells]
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge IconNextSeq500

Description

Long non-coding RNAs (lncRNAs) are a diverse category of transcripts with poor conservation and have expanded greatly in primates, particularly in their brain. We identified a lncRNA, which has acquired 16 microRNA response elements (MREs) for miR-143-3p in the Catarrhini branch of primates. This lncRNA termed LncND (neuro-development) gets expressed in neural progenitor cells and then declines in mature neurons. Binding and release of miR-143-3p, by LncND, can control the expression of Notch. Its expression is highest in radial glia cells in the ventricular and outer subventricular zones of human fetal brain. Down-regulation of LncND in neuroblastoma cells reduced cell proliferation and induced neuronal differentiation, an effect phenocopied by miR-143-3p over-expression and supported by RNA-seq analysis. These findings support a role for LncND in miRNA-mediated regulation of Notch signaling in the expansion of the neural progenitor pool of primates and hence contributing to the rapid growth of the cerebral cortex. Overall design: SHSY5Y cells treated either with miR-143-3p mimic or 100 nM of siRNA specific for LncND were sequenced on NextSeq500 platform. Scrambled siRNA or miRNA sequences were used as a negative control.

Publication Title

A Primate lncRNA Mediates Notch Signaling during Neuronal Development by Sequestering miRNA.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP059624
Primary cilium-autophagy-Nrf2 (PAN) axis links the cell cycle to neuroectoderm fate in human embryonic stem cells
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIonTorrentProton

Description

Under defined differentiation conditions human embryonic stem cells (hESCs) can be directed toward a mesendodermal (ME) or neuroectoderm (NE) fate, the first decision during hESC differentiation. Coupled with G1 lengthening a divergent ciliation pattern emerged within the first 24 hours of induced lineage specification and these changes heralded a neuroectoderm decision before any neural precursor markers were expressed. By day 2, increased ciliation in NE precursors induced autophagy that resulted in the inactivation of Nrf2. Nrf2 binds directly to upstream regions of the OCT4 and NANOG genes to promote their expression and represses NE derivation. Nrf2 suppression was sufficient to rescue poorly neurogenic iPSC lines. Only after these events have been initiated do neural precursor markers get expressed at day 4. Thus we have identified a primary cilium-autophagy-Nrf2 (PAN) axis coupled to cell cycle progression that directs hESCs toward NE. Overall design: Transcriptome analysis of hESC-derived neuroectoderm and mesendoderm cells

Publication Title

Primary Cilium-Autophagy-Nrf2 (PAN) Axis Activation Commits Human Embryonic Stem Cells to a Neuroectoderm Fate.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE102016
Expression profile from mouse lung treated with B[a]P and LPS
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Patients with inflammatory lung diseases are often additionally exposed to polycyclic aromatic hydrocarbons like B[a]P and B[a]P-induced alterations in gene expression in these patients may contribute to the development of lung cancer. Mice were intra-nasally treated with lipopolysaccharide (LPS, 20 g/mouse) to induce pulmonary inflammation and subsequently exposed to B[a]P (0.5 mg/mouse) by intratracheal instillation

Publication Title

Altered gene expression profiles in the lungs of benzo[a]pyrene-exposed mice in the presence of lipopolysaccharide-induced pulmonary inflammation.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE11769
Analysis of ectopic human endometrium and peritoneal tissues in nude mice
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Endometrial-peritoneal interactions during endometriotic lesion establishment.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE11768
Nude mouse model of endometriosis
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

The pathophysiology of endometriotic lesion development remains unclear but involves a complex interaction between ectopic endometrium and host peritoneal tissues. We hypothesised that disruption of this interaction was likely to suppress endometriotic lesion formation. We hoped to delineate the molecular and cellular dialogue between ectopic human endometrium and peritoneal tissues in nude mice, as a first step towards testing this hypothesis. Human endometrium was xenografted into nude mice and the resulting lesions were analysed using microarrays. A novel technique was developed that unambiguously determined whether RNA transcripts identified by the microarray analyses originated from human cells (endometrium) or mouse cells (stroma). Four key pathways (ubiquitin/proteosome, inflammation, tissue remodelling/repair and ras-mediated oncogenesis) were revealed, that demonstrated communication between host stromal cells and ectopic endometrium.

Publication Title

Endometrial-peritoneal interactions during endometriotic lesion establishment.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE11691
Euctopic and ectopic human endometrium (endometriosis)
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

The pathophysiology of endometriotic lesion development remains unclear but involves a complex interaction between ectopic endometrium and host peritoneal tissues. We hypothesised that disruption of this interaction was likely to suppress endometriotic lesion formation. We hoped to delineate the molecular and cellular dialogue between ectopic human endometrium and peritoneal tissues in nude mice, as a first step towards testing this hypothesis. Human endometrium was xenografted into nude mice and the resulting lesions were analysed using microarrays. A novel technique was developed that unambiguously determined whether RNA transcripts identified by the microarray analyses originated from human cells (endometrium) or mouse cells (stroma). Four key pathways (ubiquitin/proteosome, inflammation, tissue remodelling/repair and ras-mediated oncogenesis) were revealed, that demonstrated communication between host stromal cells and ectopic endometrium.

Publication Title

Endometrial-peritoneal interactions during endometriotic lesion establishment.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE23338
TGF1-driven epithelial to mesenchymal transition in human kidney cell line
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

TGFbeta is the major cytokine driver of fibrosis in the kidney and other tissue. Epithelial-mesenchymal transition has been postulated to contibrute to renal fibrosis in diseases such as diabetic nephropathy.

Publication Title

Next-generation sequencing identifies TGF-β1-associated gene expression profiles in renal epithelial cells reiterated in human diabetic nephropathy.

Sample Metadata Fields

Cell line, Time

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accession-icon SRP006912
RNA-sequencing of TGF-ß1-driven gene expression in human kidney cell line
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzer

Description

TGF-beta1 is the major cytokine driver of fibrotic scarring observed in diabetic nephropathy and other fibrosis-related diseases. RNA-sequencing offers the potential for more sensitive assessment of the TGF-ß1-driven transcriptome. Overall design: There were two treatment groups: vehicle, 48 hr TGFb1. Each treatment was carried out in triplicate. Upon quality control assessment, one TGFß1 treated sample was excluded from further analyses, leaving 3 unstimulated and 2 TGFß1 samples.

Publication Title

Next-generation sequencing identifies TGF-β1-associated gene expression profiles in renal epithelial cells reiterated in human diabetic nephropathy.

Sample Metadata Fields

No sample metadata fields

View Samples
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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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