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accession-icon GSE21155
Accelerated leukemogenesis by truncated CBFb-SMMHC defective in high-affinity binding with RUNX1
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
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Description

Dominant RUNX1 inhibition has been proposed as a common pathway for CBF-leukemia. CBFb-SMMHC, a fusion protein in human acute myeloid leukemia (AML), dominantly inhibits RUNX1 largely through its RUNX1 high-affinity binding domain (HABD). We generated knock-in mice expressing CBFb-SMMHC with a HABD deletion, CBFb-SMMHCd179-221. These mice developed leukemia highly efficiently, even though hematopoietic defects associated with Runx1-inhibition were partially rescued.

Publication Title

Accelerated leukemogenesis by truncated CBF beta-SMMHC defective in high-affinity binding with RUNX1.

Sample Metadata Fields

Specimen part

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accession-icon GSE18617
Single-cell gene expression data from Bergmann glial cells of mouse cerebellum
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
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Description

Bergmann glial cells of the vertebrate cerebellum play essential roles in the development and maintenance of cerebellar structure and function. During development, Bergmann glia provide structural support to the expanding cerebellar anlage and also serve as guides for migrating neurons (granule cells). As the cerebellum matures, Bergmann glia become important in dendritic arborization, synapse maintenance and synaptic function. The molecular mechanisms underlying these diverse and important functions of Bergmann glia remain largely unknown.

Publication Title

Identification of novel glial genes by single-cell transcriptional profiling of Bergmann glial cells from mouse cerebellum.

Sample Metadata Fields

Specimen part

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accession-icon GSE29318
Expression profile of FAC-sorted murine retinal cells
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
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Description

Microarray experiments were performed using FAC-sorted young photoreceptors to analyze their transcriptome in comparison to remaining retinal cells at same developmental stage and retinal progenitors.

Publication Title

Increased integration of transplanted CD73-positive photoreceptor precursors into adult mouse retina.

Sample Metadata Fields

Specimen part

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accession-icon GSE3203
Influenza virus infection-induced gene expression changes of regional B cells are mediated in part through type I IFN
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
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Description

Influenza virus infection-induced gene expression changes of regional B cells are mediated at least in part through type I Interferon:

Publication Title

Influenza virus infection causes global respiratory tract B cell response modulation via innate immune signals.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE27987
Differential pre-mRNA processing in Crebbp+/- mice
  • organism-icon Mus musculus
  • sample-icon 31 Downloadable Samples
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Description

The presence of unspliced transcripts in hematopoietic stem cells (HSCs) and the proposed association of CREBBP with the constitutive production of unspliced RNA and with pre-mRNA processing prompted us to examine more closely an anomaly we had noted in microarray-based gene expression studies but had previously attributed to experimental noise. We noticed that more than half of the probe sets down-regulated in Crebbp+/- fetal liver HSCs (FLHSCs) relative to wild-type (WT) mapped entirely within introns, rather than detecting exonic or spliced sequences. We therefore set out to test whether this might be evidence that reduced CREBBP levels selectively alter the generation of full-length, unspliced pre-mRNA. We also asked whether this process might be associated with differentiation since self-renewal and lineage commitment are the both responses for which HSCs are primed.

Publication Title

Inactivation of a single copy of Crebbp selectively alters pre-mRNA processing in mouse hematopoietic stem cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE21902
Expression Data from chemical induced tumors obtained from NDR1+/+, NDR1+/- and NDR1-/- mice
  • organism-icon Mus musculus
  • sample-icon 31 Downloadable Samples
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Description

Loss and heterozygosity for NDR1 predisposes mice to T-cell lymphoma development. To analyze mechanisms of tumor development in these mice chemically (ENU)-induced tumors were collected and RNA was extracted.

Publication Title

Ablation of the kinase NDR1 predisposes mice to the development of T cell lymphoma.

Sample Metadata Fields

Sex, Specimen part, Disease, Treatment

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accession-icon GSE22871
Expression data from wild-type and PPARalpha-null mice exposed to perfluorooctane sulfonate (PFOS)
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
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Description

Perfluorooctane sulfonate (PFOS) is a perfluoroalkyl acid (PFAA) and a persistent environmental contaminant found in the tissues of humans and wildlife. Although blood levels of PFOS have begun to decline, health concerns remain because of the long half-life of PFOS in humans. Like other PFAAs, such as perfluorooctanoic acid (PFOA), PFOS is an activator of peroxisome proliferator-activated receptor-alpha (PPAR) and exhibits hepatocarcinogenic potential in rodents. PFOS is also a developmental toxicant in rodents where, unlike PFOA, its mode of action is independent of PPAR. Wild-type (WT) and PPAR-null (Null) mice were dosed with 0, 3, or 10 mg/kg/day PFOS for 7 days. Animals were euthanized, livers weighed, and liver samples collected for histology and preparation of total RNA. Gene profiling was conducted using Affymetrix 430_2 microarrays. In WT mice, PFOS induced changes that were characteristic of PPAR transactivation including regulation of genes associated with lipid metabolism, peroxisome biogenesis, proteasome activation, and inflammation. PPAR-independent changes were indicated in both WT and Null mice by altered expression of genes related to lipid metabolism, inflammation, and xenobiotic metabolism. Such results are similar to prior studies done with PFOA and are consistent with modest activation of the constitutive androstane receptor (CAR) and possibly PPAR and/or PPAR/. Unique treatment-related effects were also found in Null mice including altered expression of genes associated with ribosome biogenesis, oxidative phosphorylation and cholesterol biosynthesis. Of interest was up-regulation of Cyp7a1, a gene which is under the control of various transcription regulators. Hence, in addition to its ability to modestly activate PPAR, PFOS induces a variety of off-target effects as well.

Publication Title

Gene Expression Profiling in Wild-Type and PPARα-Null Mice Exposed to Perfluorooctane Sulfonate Reveals PPARα-Independent Effects.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE18135
Gene Expression Profile of Androgen Modulated Genes in the Murine Fetal Developing Lung
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
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Description

Accumulating evidences suggest that sex affects lung development. During the fetal period, male lung maturation is delayed compared with female and surfactant production appears earlier in female than in male fetal lungs.

Publication Title

Gene expression profile of androgen modulated genes in the murine fetal developing lung.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE26912
Inflammation driven by tumor-specific Th1 cells protects against B-cell cancer
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

The immune system can both promote and suppress cancer. Chronic inflammation and proinflammatory cytokines such as interleukin (IL)-1 and IL-6 are considered tumor-promoting. In contrast, the exact nature of protective antitumor immunity remains obscure. In this study, we have quantified locally secreted cytokines during primary immune responses against myeloma and B-cell lymphoma in mice. Strikingly, successful cancer immunosurveillance mediated by tumor-specific CD4+ T cells was consistently associated with elevated local levels of both proinflammatory (IL-1aplha, IL-1beta, and IL-6) and T helper 1 (Th1)-associated cytokines (interferon-alpha, IL-2, IL-12). Cancer eradication was achieved by a collaboration between tumor-specific Th1 cells and tumor-infiltrating, antigen-presenting macrophages. Th1 cells induced secretion of IL-1? and IL-6 by macrophages. Th1-derived interferon-? was shown to render macrophages directly cytotoxic to cancer cells, and to induce macrophages to secrete the angiostatic chemokines CXCL9/MIG and CXCL10/IP-10. Thus, inflammation, when driven by tumor-specific Th1 cells, may prevent rather than promote cancer.

Publication Title

Inflammation driven by tumour-specific Th1 cells protects against B-cell cancer.

Sample Metadata Fields

Specimen part

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accession-icon GSE21224
Transcriptional ontogeny of the developing liver
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
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Description

We characterized gene expression changes in the developing mouse liver at gestational days (GD) 11.5, 12.5, 13.5, 14.5, 16.5, and 19.5 and in the neonate (postnatal day (PND) 7 and 30) using full-genome microarrays and compared these changes to that in the adult liver. The fetal liver, and to a lesser extent the neonatal liver, exhibited dramatic differences in gene expression compared to adults. Canonical pathway analysis of the fetal liver signature demonstrated increases in functions important in cell replication and DNA fidelity whereas most metabolic pathways of intermediary metabolism were suppressed. Comparison of the dataset to a number of previously published datasets revealed 1) a striking similarity between the fetal liver and that of the pancreas in both mice and humans, 2) a nucleated erythrocyte signature in the fetus and 3) suppression of most xenobiotic metabolism genes throughout development, except a number of transporters associated with expression in hematopoietic cells.

Publication Title

Transcriptional ontogeny of the developing liver.

Sample Metadata Fields

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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