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accession-icon GSE49053
Differentiation defective phenotypes revealed by large scale analyses of human pluripotent stem cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Differentiation-defective phenotypes revealed by large-scale analyses of human pluripotent stem cells.

Alternate Accession IDs

E-GEOD-49053

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE42449
Exon array analysis for SFEBq differentiation-defective clones and good clones
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

It remains controversial whether human induced pluripotent stem cells (hiPSCs) are distinct from human embryonic stem cells (hESCs) in their molecular signatures and differentiation properties. We examined the gene expression and DNA methylation of 49 hiPSC and 10 hESC lines and identified no molecular signatures that distinguished hiPSCs from hESCs. Comparisons of the in vitro directed neural differentiation of 40 hiPSC and four hESC lines showed that most hiPSC clones were comparable to hESCs. However, in seven hiPSC clones, significant amount of undifferentiated cells persisted even after neural differentiation and resulted in teratoma formation when transplantated into mouse brains. These differentiation-defective hiPSC clones were marked by higher expression of several genes, including those expressed from long terminal repeats of human endogenous retroviruses. These data demonstrated that many hiPSC clones are indistinguishable from hESCs, while some defective hiPSC clones need to be eliminated prior to their application for regenerative medicine.

Publication Title

Differentiation-defective phenotypes revealed by large-scale analyses of human pluripotent stem cells.

Alternate Accession IDs

E-GEOD-42449

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE17939
MEK5D-transfected HUVEC
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We expressed a constitutively active mutant of MEK5 (MEK5D) in human primary endothelial cells (EC) to study the transcriptional and functional responses to Erk5 activation under static conditions.

Publication Title

Erk5 activation elicits a vasoprotective endothelial phenotype via induction of Kruppel-like factor 4 (KLF4).

Alternate Accession IDs

E-GEOD-17939

Sample Metadata Fields

Cell line

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accession-icon GSE37056
Expression data from fosb gene modified mouse
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

To examine fosB regulation of neurogenesis, depression and epilepsy, we compared the gene expression profiles of wild type, fosBd/d and fosB-null mice by microarray analysis.

Publication Title

fosB-null mice display impaired adult hippocampal neurogenesis and spontaneous epilepsy with depressive behavior.

Alternate Accession IDs

E-GEOD-37056

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon GSE35011
PPARg agonists induce a white-to-brown fat conversion through stabilization of PRDM16 protein
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Brown adipose tissue dissipates energy through heat and functions as a defense against cold and obesity. PPAR ligands have been shown to induce the browning of white adipocytes; however, the underlying mechanisms remain unclear. Here we show that PPAR ligands require full agonism to induce a brown fat gene program preferentially in subcutaneous white adipose. These effects require expression of PRDM16, a factor that controls the development of classical brown fat. Depletion of PRDM16 blunts the effects of the PPAR agonist rosiglitazone on the induced brown fat gene program. Conversely, PRDM16 and rosiglitazone synergistically activate the brown fat gene program in vivo. This synergy is tightly associated with an increased accumulation of PRDM16 protein, due in large measure to an increase in the half-life of the protein in agonist treated cells. Identifying compounds that stabilize PRDM16 protein may represent a novel therapeutic pathway for the treatment of obesity and diabetes.

Publication Title

PPARγ agonists induce a white-to-brown fat conversion through stabilization of PRDM16 protein.

Alternate Accession IDs

E-GEOD-35011

Sample Metadata Fields

Sex

View Samples
accession-icon GSE103941
Expression data from mice liver drinking Hydrogen water
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Liver RNA samples from C57BL6 mice drinking Hydrogen water for 4 weeks

Publication Title

Molecular hydrogen upregulates heat shock response and collagen biosynthesis, and downregulates cell cycles: meta-analyses of gene expression profiles.

Alternate Accession IDs

E-GEOD-103941

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE18474
A novel metabolic monitoring system identified nutrition-mediated microbial interactions
  • organism-icon Escherichia coli, Bifidobacterium longum
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

"Omics" technologies have been developed to understand the whole complex microbial systems; however, most omics studies reported so far were utilized to analyze the living matters of single-species. To understand the cell-cell interaction in the gut microbial complex, we selected to examine the interaction of Escherichia coli O157:H7 (O157) and Bifidobacterium longum (BL), known as a pathogenic and a commensal bacteria, as a first step for understanding the whole gut microbial complex. We have developed a novel time-lapse 2D-NMR metabolic profiling system in order to measure the extracellular metabolites, which are considered a key factor to understand the bacterial crosstalk. Furthermore, in combination with transcriptome and proteome analysis, we found that the relationship between BL and O157 could be partially regarded as the producer and the consumer of nutrients, especially in the case of serine and aspartate metabolism. These findings suggest that our novel profiling systems could be a powerful tool toward understanding crosstalk of the whole microbial complex such as the gut, industrial bioreactors or environmental microbial communities.

Publication Title

Dynamic omics approach identifies nutrition-mediated microbial interactions.

Alternate Accession IDs

E-GEOD-18474

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE16081
Gallus gallus bursal FAE and IFE
  • organism-icon Gallus gallus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Chicken Genome Array (chicken)

Description

A minor population of M cells within the follicle-associated epithelium (FAE) of intestinal Peyers patches (PP) serves as a major portal for entry of exogenous antigens. Characterization of the mammalian M cells, including identification of M-cell surface molecules used for bacterial uptake, has been hampered by their relative rarity. In contrast, M cells constitute virtually all of the FAE cells in the avian bursa of Fabricius. We therefore performed comparative gene expression profiling of chicken and murine FAE to identify commonly expressed genes by M cells in both species. The comprehensive transcriptome analysis revealed that 28 genes were commonly up-regulated in FAE from both species. In situ hybridization (ISH) revealed that annexin A10 (Anxa10) mRNA was scattered in FAE, and co-localized with Ulex europaeus agglutinin-1(UEA-1) that binds to M cells. Whole-mount immunostaining also revealed that cellular prion protein (PrPC) was expressed on the luminal side of the apical plasma membrane of M cells, and co-localized with grycoprotein2 (GP2) that recognizes only M cells in murine PP. Taken together, we found new M-cell-specific molecules by using comprehensive transcriptome analysis. These molecules conserved in M cells from both species might play critical roles in M-cell function and/or differentiation.

Publication Title

New approach for m-cell-specific molecules screening by comprehensive transcriptome analysis.

Alternate Accession IDs

E-GEOD-16081

Sample Metadata Fields

Age, Specimen part, Disease, Disease stage

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accession-icon GSE27583
mRNA decay analysis in the mouse myoblast cell line, C2C12 cells treated with conrtol-, Cugbp1- or Mbnl1-siRNA
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

CUGBP1 and MBNL1 are developmentally regulated RNA-binding proteins that are causally associated with myotonic dystrophy type 1. Using HITS-CLIP anlysis, we found CUGBP1 and MBNL1 preferentially bind to alternatively spliced introns and exons, as well as to the 3' UTRs.

Publication Title

CUGBP1 and MBNL1 preferentially bind to 3' UTRs and facilitate mRNA decay.

Alternate Accession IDs

E-GEOD-27583

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon SRP200067
Constitutive CD8 expression drives innate CD8+ T cell differentiation via induction of iNKT2 subset
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1500

Description

Constitutive CD8 expression drives innate CD8+ T cell differentiation via induction of iNKT2 subset. Overall design: Analysis of RNA from Cd8ab transgenic mice by RNA-seq.

Publication Title

Constitutive CD8 expression drives innate CD8<sup>+</sup> T-cell differentiation via induction of iNKT2 cells.

Alternate Accession IDs

GSE132059

Sample Metadata Fields

Specimen part, Subject

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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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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