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accession-icon GSE6867
Expression data in the absence of Notch1 in hair follicles
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
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Description

Notch1 deficient hair matrix keratinocytes have lower mitotic rates, resulting in smaller follicles with fewer cells. In addition, the ratio of melanocytes to keratinocytes is greatly reduced. Microarray was performed to study downstream mechanism of Notch1-deficiency

Publication Title

Bi-compartmental communication contributes to the opposite proliferative behavior of Notch1-deficient hair follicle and epidermal keratinocytes.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE27901
Transactivation-deficient p53 Mutants in Ras-induced Cellular Senescence
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
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Description

As a critical cellular stress sensor, p53 mediates a variety of defensive processes including cell-cycle arrest, apoptosis, and senescence to prevent propagation of hyperproliferative cells or cells with a damaged genome, hence the formation of neoplasia. Transactivation of downstream genes plays an important while sometimes controversial role in regulating these cellular processes. To evaluate the dependence on transcriptional activation in p53s activities, we generated genetically-modified mouse lines carrying mutations in the transactivation domains (TADs) of p53. These transactivatio-deficient mutants serve as unique reagents to probe the dependence on robust transactivation in p53-mediated cellular functions, as well as the underneath mechanisms. To identify genes differentially regulated by these p53 mutants, we performed gene expression profiling analysis on mouse embryonic fibroblast cells (MEFs) from these mice in the context of oncogenic Ras-induced premature cellular senescence.

Publication Title

Distinct p53 transcriptional programs dictate acute DNA-damage responses and tumor suppression.

Sample Metadata Fields

Specimen part

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accession-icon GSE20523
Immunoregulatory actions of T cell PPAR g at the colonic mucosa
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
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Description

BACKGROUND: Peroxisome proliferator-activated receptor g (PPAR g) is a nuclear receptor whose activation has been shown to modulate macrophage and epithelial cell-mediated inflammation. The objective of this study was to use a systems approach for investigating the mechanism by which the deletion of PPAR g in T cells modulates the severity of dextran-sodium sulfate (DSS)-induced colitis, immune cell distribution and global gene expression.

Publication Title

The role of T cell PPAR gamma in mice with experimental inflammatory bowel disease.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE42008
Expression data from NcGFP ki/+, NcGFP ki/ki and wt (W4) ES cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
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Description

We generated a gene replacement allele of the E-cadherin locus that express an N-cadherin-GFP fusion in ES cells. Expression profiles of homozygous and heterozygous knock-in ES cells were analyzed in comparison to wt ES cells.

Publication Title

Adhesion, but not a specific cadherin code, is indispensable for ES cell and induced pluripotency.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE20621
Immunoregulatory actions of epithelial cell PPAR g at the colonic mucosa
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon

Description

BACKGROUND: Peroxisome proliferator-activated receptor g (PPAR g) is a nuclear receptor whose activation has been shown to modulate macrophage and epithelial cell-mediated inflammation. The objective of this study was to use a systems approach for investigating the mechanism by which the deletion of PPAR g in epithelial cells modulates the severity of dextran-sodium sulfate (DSS)-induced colitis, immune cell distribution and global gene expression.

Publication Title

Immunoregulatory actions of epithelial cell PPAR gamma at the colonic mucosa of mice with experimental inflammatory bowel disease.

Sample Metadata Fields

Specimen part

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accession-icon GSE16207
Expression data from mouse liver infected with Ft LVS (without or with LPS pretreatment)
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
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Description

Background: It has been shown previously that administration of Francisella tularensis (Ft) LVS lipopolysaccharide (LPS) protects mice against subsequent challenge with Ft LVS and blunts the pro-inflammatory cytokine response.

Publication Title

Modulation of hepatic PPAR expression during Ft LVS LPS-induced protection from Francisella tularensis LVS infection.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE30834
Influence of C/EBP 3'UTR on RasV12 induced gene expression
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

C/EBPb is an auto-repressed protein that becomes posttranslationally activated by Ras-MEK-ERK signalling. C/EBPb is required for oncogene-induced senescence (OIS) of primary fibroblasts, but also displays pro-oncogenic functions in many tumour cells. Here, we show that C/EBPb activation by H-RasV12 is suppressed in immortalized/transformed cells, but not in primary cells, by its 30 untranslated region (30UTR). 30UTR sequences inhibited Ras-induced cytostatic activity of C/EBPb, DNA binding, transactivation, phosphorylation, and homodimerization, without significantly affecting protein expression. The 30UTR suppressed induction of senescence-associated C/EBPb target genes, while promoting expression of genes linked to cancers and TGFb signalling. An AU-rich element (ARE) and its cognate RNA-binding protein, HuR, were required for 30UTR inhibition. These components also excluded the Cebpb mRNA from a perinuclear cytoplasmic region that contains activated ERK1/2, indicating that the site of C/EBPb translation controls de-repression by Ras signalling. Notably, 30UTR inhibition and Cebpb mRNA compartmentalization were absent in primary fibroblasts, allowing Ras-induced C/EBPb activation and OIS to proceed. Our findings reveal a novel mechanism whereby non-coding mRNA sequences selectively regulate C/EBPb activity and suppress its anti-oncogenic functions.

Publication Title

3'UTR elements inhibit Ras-induced C/EBPβ post-translational activation and senescence in tumour cells.

Sample Metadata Fields

Cell line

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accession-icon GSE71270
Creb overexpression induces leukemia in zebrafish by blocking myeloid differentiation process
  • organism-icon Danio rerio
  • sample-icon 1 Downloadable Sample
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Description

To examine the role of CREB overexpression in hematopoiesis, we created a model of leukemia in zebrafish by overexpressing the human CREB in the myeloid hematopoietic lineage. Whole transcriptome analysis of kidney-marrow revealed 171 genes differently expressed between CREB- and control-zebrafish (five per group). Interestingly, the integration of this signature with human deposited data revealed that this tumor resembled a human AML at transcriptome level.

Publication Title

CREB engages C/EBPδ to initiate leukemogenesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE28736
BATF knockout B cells
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

compare wild type and Batf-/- B cells activated for 0 1 or 2 days in vitro.

Publication Title

The transcription factor BATF controls the global regulators of class-switch recombination in both B cells and T cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE70164
De novo generation of somatic stem cells from differentiated cells [mammary]
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon

Description

To investigate the role of YAP/TAZ as factors able to convert differentiated cells into stem cells of the same tissue, we compared the expression profiles of mammary organoids (yOrg) obtained by doxycycline-inducible expression of YAP in luminal differentiated mammary cells with original luminal differentiated mammary cells (Lum) and organoids from native mammary stem cells (Org).

Publication Title

Induction of Expandable Tissue-Specific Stem/Progenitor Cells through Transient Expression of YAP/TAZ.

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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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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