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accession-icon GSE62691
Gene expression of resting memory, resting naive and in vitro activated memory CD8+CD127+ T cells from spleen and bone marrow (BM)
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon

Description

To understand differences between resting and activated memory CD8+ T cells, we compared the global gene expression of ex vivo isolated naive and spleen and BM memory cells to in vitro activated spleen and BM memory cells.

Publication Title

Memory CD8(+) T cells colocalize with IL-7(+) stromal cells in bone marrow and rest in terms of proliferation and transcription.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE66370
Expression and role of Galectins 1 and 3 in the lesioned brain
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Astrocytes react to brain injury in a heterogeneous manner with only a subset resuming proliferation and acquiring in vitro neural stem cell properties. In order to identify novel regulators of this astrocyte subset, we performed a genome-wide expression analysis of reactive astrocytes isolated 5 days after stab wound injury from the adult mouse cerebral cortex. The expression pattern was compared with astrocytes from normal cortex and adult neural stem cells isolated from the sub-ependymal zone (GSE18765). These comparisons revealed a set of genes up-regulated both in neurogenic neural stem cells and reactive astrocytes, including the lectins Galectin-1 and -3. These results, as well as the pattern of Galectin expression in the lesioned brain, led us to examine the functional significance of these lectins in brains of Galectin-1/3 double-knockout mice.

Publication Title

Astrocyte reactivity after brain injury-: The role of galectins 1 and 3.

Sample Metadata Fields

Sex, Specimen part, Treatment, Time

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accession-icon GSE27261
Dmrt1 (doublesex and mab-3 related transcription factor 1) conditional knockout expression analysis of P28 testes
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Dmrt1 (doublesex and mab-3 related transcription factor 1) is a conserved transcriptional regulator of male differentiation required for testicular development in vertebrates. This study examines the result of conditional removal of Dmrt1 from Sertoli cells in P28 testis tissue.

Publication Title

DMRT1 prevents female reprogramming in the postnatal mammalian testis.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE38754
Temporal changes of gene expression in mouse heart, kidney and lung during juvenile growth
  • organism-icon Mus musculus
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon

Description

Temporal changes of gene expression from 1-wk- to 4-wk and 8-wk-old mouse in heart, kidney and lung. Mammalian somatic growth is rapid in early postnatal life but then slows and eventually ceases in multiple tissues. We hypothesized that there exists a postnatal gene expression program that is common to multiple tissues and is responsible for this coordinate growth deceleration. Consistent with this hypothesis, microarray analysis identified >1600 genes that were regulated with age coordinately in kidney, lung, and heart of juvenile mice, including many genes that regulate proliferation. As examples, we focused on three growth-promoting genes, Igf2, Mest, and Peg3, that were markedly downregulated with age. We conclude that there exists an extensive genetic program occurring during postnatal life. Many of the involved genes are regulated coordinately in multiple organs, including many genes that regulate cell proliferation. At least some of these are themselves apparently regulated by growth, suggesting that, in the embryo, a gene expression pattern is established that allows for rapid somatic growth of multiple tissues but then, during postnatal life, this growth leads to negative-feedback changes in gene expression that in turn slow and eventually halt somatic growth, thus imposing a fundamental limit on adult body size.

Publication Title

An extensive genetic program occurring during postnatal growth in multiple tissues.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE25140
Prostate specific Pten deletion, Pten-Smad4 deletion, and Pten-p53 deletion
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon

Description

We used microarrays to detail the global gene expression and identified differentially expressed gene list between wild-type anterior prostates and Ptenpc-/- anterior prostates, Ptenpc-/-Smad4pc-/- and Ptenpc-/- anterior prostates, Ptenpc-/-p53pc-/- and Ptenpc-/- anterior prostates at 15 weeks of age.

Publication Title

SMAD4-dependent barrier constrains prostate cancer growth and metastatic progression.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE16387
Licensing of PPARg-regulated gene expression by IL-4-induced alternative macrophage activation
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

STAT6 transcription factor is a facilitator of the nuclear receptor PPARγ-regulated gene expression in macrophages and dendritic cells.

Sample Metadata Fields

Specimen part, Treatment, Subject, Time

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accession-icon GSE25088
PPARg and IL-4-induced gene expression data from wild-type and STAT6 knockout mouse bone marrow-derived macrophages
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

C57Bl/6 wild-type and STAT6 KO mice were used to study PPARg and IL-4 signaling. Bone marrow of 3 mice per group was isolated and differentiated to macrophages with M-CSF (20 ng/ml). 20 ng/ml IL-4 was used to induce alternative macrophage activation and 1 uM Rosiglitazone (RSG) was used to activate PPARg. From each mouse 4 samples were generated: 1. M-CSF, 2. M-CSF+RSG, 3. IL-4 and 4. IL-4+RSG. All compounds were added throughout the whole differentiation process, and frech media was added every other day. Control cells were treated with vehicle (DMSO:ethanol). After 10 days, RNA was isolated and gene expression profiles were analyzed using Mouse Genome 430 2.0 microarrays from Affymetrix.

Publication Title

STAT6 transcription factor is a facilitator of the nuclear receptor PPARγ-regulated gene expression in macrophages and dendritic cells.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE18396
Dmrt1 (doublesex and mab-3 related transcription factor 1) knockout expression analyses in E13.5 testes in S6 background
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Dmrt1 (doublesex and mab-3 related transcription factor 1) is a conserved transcriptional regulator of male differentiation required for testicular development in vertebrates. In mice of the 129Sv strain, loss of Dmrt1 causes a high incidence of teratomas. Mutant 129Sv germ cells undergo apparently normal differentiation up to embryonic day 13.5 (E13.5), but some cells fail to arrest mitosis and ectopically express pluripotency markers. Expression analysis and chromatin immunoprecipitation identified DMRT1 target genes whose misexpression may underly teratoma formation.

Publication Title

The DM domain protein DMRT1 is a dose-sensitive regulator of fetal germ cell proliferation and pluripotency.

Sample Metadata Fields

Specimen part

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accession-icon GSE25828
Pten deficiency cooperates with KrasG12D to activate NFkB pathway promoting the development of malignant pancreatic ductal adenocarcinoma
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

Almost all human pancreatic ductal adenocarcinomas (PDACs) are driven by oncogenic Kras and the progression of the disease is characterized by the serial appearance of certain genetic lesions. Mouse models have convincingly shown that Kras mutation induces classical PanIN lesions that can progress to PDAC in the appropriate tumor suppressor background. However, the cooperative mechanism between mutant Kras-dependent signaling surrogates and other oncogenic pathways remains to be fully elucidated in order to devise better therapeutic strategy. Mounting evidence PTEN/PI3K perturbation on PDAC tumorigenesis, we observed frequent PTEN inactivation at both genomic and histopathological levels in primary human PDAC samples. The importance of PTEN/PI3K pathway during the development of PDAC was further supported by genetic studies demonstrating that Pten deficiency in cooperation with Kras activation accelerated the formation of invasive PDAC. Mechanistically, combined Kras mutation and Pten inactivation leads to NFkB activation and subsequent induction of cytokine pathways, accompanied with strong stromal activation and immune cell infiltration. Therefore, PTEN/PI3K pathway dictates the activity of NFkB network and serves as a major surrogate during Kras-mediated pancreatic tumorigenesis.

Publication Title

PTEN is a major tumor suppressor in pancreatic ductal adenocarcinoma and regulates an NF-κB-cytokine network.

Sample Metadata Fields

Specimen part

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accession-icon GSE26299
Gene expression profiling in DBA/2J glaucoma
  • organism-icon Mus musculus
  • sample-icon 107 Downloadable Samples
  • Technology Badge Icon

Description

In this study that was specifically designed to identify early stages of glaucoma in DBA/2J mice, we used genome-wide expression profiling and a series of computational methods. Our methods successfully subdivided eyes with no detectable glaucoma by conventional assays into molecularly defined stages of disease. These stages represent a temporally ordered sequence of glaucoma states. Using an array of tools, we then determined networks and biological processes that are altered at these early stages. Our strategy proved very sensitive, suggesting that similar approaches will be valuable for uncovering early processes in other complex, later-onset diseases. Early changes included upregulation of both the complement cascade and endothelin system, and so we tested the therapeutic value of separately inhibiting them. Mice with a mutation in the complement component 1a gene (C1qa) were robustly protected from glaucoma with the protection being among the greatest reported. Similarly, inhibition of the endothelin system was strongly protective. Since EDN2 is potently vasoconstrictive and was produced by microglial/macrophages, our data provide a novel link between these cell types and vascular dysfunction in glaucoma. Targeting early events such as the upregulation of the complement and endothelin pathways may provide effective new treatments for human glaucoma.

Publication Title

Molecular clustering identifies complement and endothelin induction as early events in a mouse model of glaucoma.

Sample Metadata Fields

Sex, Age, Specimen part

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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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