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accession-icon GSE64896
Gene expression of distinct lung dendritic cell subsets
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
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Description

Pulmonary dendritic cells are heterogenous cells comprise four distinct subsets including two conventional dendritic cell subsets, CD103+ and CD11bhiCD14lo cells, and two monocyte-derived dendritic cell subsets. Their functions in terms of migration and T cell activation are distinct, but genes regulating their features are to be determined.

Publication Title

Complement receptor C5aR1/CD88 and dipeptidyl peptidase-4/CD26 define distinct hematopoietic lineages of dendritic cells.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE17101
Expression profiles of mouse glioma-initiating cell-like subclones
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
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Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Sox11 prevents tumorigenesis of glioma-initiating cells by inducing neuronal differentiation.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE17076
Expression profiling of sox11-expressing glioma-initiating cell-like cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
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Description

To identify factors involved in tumorigenicity of glioma-initiating cells (GICs), we compared gene expression in GIC-like cells with and without sox11 expression.

Publication Title

Sox11 prevents tumorigenesis of glioma-initiating cells by inducing neuronal differentiation.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE17062
Expression profiling of mouse glioma-initiating cell-like cells (GICs) and non-GICs
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
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Description

To identify factors involved in glioma-initiating cells (GICs), we compared gene expression between GIC-like cells and non-GICs.

Publication Title

Sox11 prevents tumorigenesis of glioma-initiating cells by inducing neuronal differentiation.

Sample Metadata Fields

Specimen part

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accession-icon GSE64154
Expression data from Fbxl10 overexpressing 3T3-L1 cells
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
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Description

Target genes of Fbxl10 during 3T3-L1 adipogenesis was analyzed

Publication Title

The FBXL10/KDM2B scaffolding protein associates with novel polycomb repressive complex-1 to regulate adipogenesis.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE16266
Identification of inflammatory genes suppressed by heat shock
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
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Description

To clarify inflammatory genes whose expression is suppressed at high temperatures, we performed comprehensive analysis of gene expression by using a DNA microarray. Two independent primary cultures of mouse embryo fibroblasts (MEF1 and MEF2) were treated with LPS for 4 hours, or treated with LPS for 4 hours after the pretreatment with heat shock at 42C for 1 hour, and we identified 100 genes that undergo more than a 3-fold increase with LPS treatment. Remarkably, 86 genes (86%) underwent less than a 2-fold increase after combined treatments with heat shock and LPS in MEF1 and MEF2 cells.

Publication Title

Heat shock transcription factor 1 inhibits expression of IL-6 through activating transcription factor 3.

Sample Metadata Fields

Specimen part

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accession-icon GSE18281
Spatial mapping of thymic stromal microenvironments reveals unique features influencing T lymphoid differentiation
  • organism-icon Mus musculus
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon

Description

Interaction of hematopoietic progenitors with the thymic stromal microenvironment induces them to proliferate, adopt the T cell fate, and asymmetrically diverge into multiple T lineages. Progenitors at various developmental stages are stratified among different regions of the thymus, implying that the corresponding microenvironments differ from one another, and provide unique sets of signals to progenitors migrating between them. The nature of these differences remains undefined. Here we use novel physical and computational approaches to characterize these stromal subregions, distinguishing gene expression in microdissected tissues from that of their lymphoid constituents. Using this approach, we comprehensively map gene expression in functionally distinct stromal microenvironments, and identify clusters of genes that define each region. Quite unexpectedly, we find that the central cortex lacks distinctive features of its own, and instead appears to function by sequestering unique microenvironments found at the cortical extremities, and modulating the relative proximity of progenitors moving between them.

Publication Title

Spatial mapping of thymic stromal microenvironments reveals unique features influencing T lymphoid differentiation.

Sample Metadata Fields

Specimen part

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accession-icon GSE98761
DNA microarray analysis of Jmjd1a and/or Jmjd1b knockout embryonic stem cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
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Description

Histone H3 lysine 9 (H3K9) methylation is an epigenetic mark of transcriptionally repressed chromatin. During mammalian development, H3K9 methylation levels seem to be spatiotemporally regulated by the opposing activities of methyltransferases and demethylases to govern correct gene expression. However, the combination(s) of H3K9 methyltransferase(s) and demethylase(s) that contribute to this regulation and the genes regulated by them remain unclear. Herein, we demonstrate the essential roles of H3K9 demethylases Jmjd1a and Jmjd1b in the embryogenesis and viability control of embryonic stem (ES) cells. Mouse embryos lacking Jmjd1a/Jmjd1b died after implantation. Depletion of Jmjd1a/Jmjd1b in mouse ES cells induced rapid cell death accompanied with a massive increase in H3K9 methylation. Jmjd1a/Jmjd1b depletion induced an increase in H3K9 methylation in the gene-rich regions of the chromosomes, indicating that Jmjd1a/Jmjd1b removes H3K9 methylation marks in the euchromatin. Importantly, the additional disruption of the H3K9 methyltransferase G9a in a Jmjd1a/Jmjd1b-deficient background rescued not only the H3K9 hypermethylation phenotype but also the cell death phenotype. We also found that Jmjd1a/Jmjd1b removes H3K9 methylation marks deposited by G9a in the Oct4 and Ccnd1 loci to activate transcription. In conclusion, Jmjd1a/Jmjd1b ensures ES cell viability by antagonizing G9a-mediated H3K9 hypermethylation in the gene-rich euchromatin.

Publication Title

Combined Loss of JMJD1A and JMJD1B Reveals Critical Roles for H3K9 Demethylation in the Maintenance of Embryonic Stem Cells and Early Embryogenesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE25252
Comparison of expression profiles of Foxp3(+)epigenetics(-) T cells, Foxp3(-)epigenetics(+) T cells, and Foxp3(+)epigenetics(+) T cells
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

Analysis of Foxp3(+)epigenetics(-) T cells, Foxp3(-)epigenetics(+) T cells, and Foxp3(+)epigenetics(+) T cells. Results indicate regulatory T cell (Treg) ontogenesis requires two independent processes, expression of the transcription factor Foxp3 and establishment of Treg epigenetic programs induced by T cell receptor (TCR) stimulation.

Publication Title

T cell receptor stimulation-induced epigenetic changes and Foxp3 expression are independent and complementary events required for Treg cell development.

Sample Metadata Fields

Specimen part

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accession-icon GSE109839
Effect of LSD1 knockdown on differentiating C2C12 myoblasts
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
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Description

Analysis of differentiating LSD1-KD C2C12 myoblasts. We found LSD1 is an important regulator of oxidative phenotypes in skeletal muscle cells.

Publication Title

LSD1 mediates metabolic reprogramming by glucocorticoids during myogenic differentiation.

Sample Metadata Fields

Specimen part, Cell line

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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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