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accession-icon GSE23308
Effect of Mineralocorticoid Receptor deletion on glucocorticoid signalling in the macropahge
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Inappropriate excess of the steroid hormone aldosterone, which is a mineralocorticoid receptor (MR) agonist, is associated with increased inflammation and risk of cardiovascular disease. MR antagonists are cardioprotective and antiinflammatory in vivo, and evidence suggests that they mediate these effects in part by aldosterone- independent mechanisms.

Publication Title

Myeloid mineralocorticoid receptor controls macrophage polarization and cardiovascular hypertrophy and remodeling in mice.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE19693
STAR RNA-binding protein, Quaking, suppresses cancer via regulation of microRNA
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon

Description

MicroRNAs have emerged as major genetic elements in the genesis and suppression of cancer. Here, multi-dimensional cancer genome analysis and validation has defined a novel Glioblastoma Multiforme (GBM) tumor suppressor pathway and mechanism of action centered on Quaking (QK), a member of the STAR family of RNA-binding proteins. Combined functional, biochemical and computational studies establish that p53 directly regulates QK gene expression, QK protein binds and stabilizes miR-20a of the cancer-relevant miR-17-92 cluster, and miR-20a in turn functions to regulate TGFR2 and the TGF signaling network. Linkage of these pathway components is supported by their genome and expression status across GBM specimens and by their gain- and loss-of-function interactions in in vitro and in vivo complementation studies. This p53-QK-miR-20a axis expands our understanding of the p53 tumor suppression network in cancer and reveals a novel tumor suppression mechanism involving regulation of specific cancer-relevant microRNAs.

Publication Title

STAR RNA-binding protein Quaking suppresses cancer via stabilization of specific miRNA.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE19687
shGFP- and shQk-transduced Ink4a/Arf-/- Pten-/- primary mouse astrocytes
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Identify potential QK-regulated mRNAs and linked pathways by comparing the transcriptional profiles of shGFP- and shQK-transduced Ink4a/Arf-/- Pten-/- primary mouse astrocytes

Publication Title

STAR RNA-binding protein Quaking suppresses cancer via stabilization of specific miRNA.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE19689
QK-knockdown Ink4a/Arf-/- Pten-/- mouse astrocytes transduced with miR-20a or scrambled non-targeting microRNA (miR-NT)
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Identify potential miR-20a regulated mRNAs and linked pathways in the setting of QK knockdown by comparing the transcriptional profiles of shQK-transduced primary mouse Ink4a/Arf-/- Pten-/- astrocytes together with miR-20a or a scrambled miRNA control (miR-NT)

Publication Title

STAR RNA-binding protein Quaking suppresses cancer via stabilization of specific miRNA.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE23161
Beta cell overexpression of HSD11B1 in high fat fed mice
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

To model the potential diabetogenic effects of higher level of HSD11B1 in b-cells of the pancreas in vivo, we created a transgenic model overexpressing HSD11B1 under the mouse insulin I promoter (MIP-HSD1) in diabetes-prone C57Bl/KsJ mice. KsJ wild type and MIP-HSD1 heterozygous mice have been high fat fed for 12 weeks. Pancreata have been perfused with collagenase and islets isolated by hand picking. Isolated islets (around 500) coming from at least 3 mice (around 200/mice) have been directly lysed in Trizol. Total RNA have been extracted by Trizol plus RNA Purification Kit (invitrogen).

Publication Title

Optimal elevation of β-cell 11β-hydroxysteroid dehydrogenase type 1 is a compensatory mechanism that prevents high-fat diet-induced β-cell failure.

Sample Metadata Fields

Specimen part

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accession-icon GSE30701
In vivo Gene Expression Profiling of Retina Post-Intravitreal Injections of Dexamethasone and Triamcinolone at Clinically Relevant Time Points for Patient Care
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

PURPOSE To identify retinal genes and their relevant expression pathways affected by intravitreal injections of dexamethasone and triamcinolone acetonide in mice at clinically relevant time points for patient care.

Publication Title

In vivo gene expression profiling of retina postintravitreal injections of dexamethasone and triamcinolone at clinically relevant time points for patient care.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE24574
Expression data from BCL6-YFP-positive Tfh cells, BCL6-YFP-negative Tfh cells, non-Tfh cells, and nave helper T cells.
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

We found that a number of Tfh cells downmodulated BCL6 protein after their development, and we sought to compare the gene expression between BCL6-hi Tfh cells and BCL6-low Tfh cells.

Publication Title

Bcl6 protein expression shapes pre-germinal center B cell dynamics and follicular helper T cell heterogeneity.

Sample Metadata Fields

Specimen part

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accession-icon GSE10964
Virus-Induced Airway Disease in Mice (C57BL/6J, d21/d49)
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon

Description

Analysis of gene expression in lungs of C57BL/6J mice that develop chronic airway disease phenotypes after a single Sendai virus infection, compared with mice treated with UV-inactivated virus.

Publication Title

Persistent activation of an innate immune response translates respiratory viral infection into chronic lung disease.

Sample Metadata Fields

Sex, Time

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accession-icon GSE67358
Promotion of pancreatic cancer metastasis by mutant p53
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon

Description

The TP53 transcription factor is frequently mutated at later stages of epithelial cancers, indicating a possible role in their invasion and metastasis. Importantly, in most cases rather than a simple loss of function p53 mutation, point mutations of p53 accumulate at the protein level and may have dominant negative functions. This study analyses gene expression differences between mice harbouring p53 mutation who do and do not develop metastasis.

Publication Title

Targeting the LOX/hypoxia axis reverses many of the features that make pancreatic cancer deadly: inhibition of LOX abrogates metastasis and enhances drug efficacy.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE9249
Gene expression analysis of B-NHL from MYC, MYC/IHABCL6, MYC/AIDKO and MYC/IHABCL6/AIDKO mouse models
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Most human B cell lymphomas (B-NHL) are derived from germinal centers (GCs), the structure where B-cells undergo class switch recombination (CSR) and somatic hypermutation (SHM) and are selected for high-affinity antibody production. The pathogenesis of B-NHL is associated with distinct genetic lesions, including chromosomal translocations and aberrant somatic hypermutation, which appear to arise from mistakes occurring during CSR and SHM. To ascertain the role of CSR and SHM in lymphomagenesis, we crossed three oncogene-driven (MYC, BCL6, MYC/BCL6) mouse models of B cell lymphoma with mice lacking activation-induced cytidine deaminase (AID), the enzyme required for both processes.

Publication Title

AID is required for germinal center-derived lymphomagenesis.

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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