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accession-icon GSE62385
Intermittent Hypoxia ageing
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon

Description

Expression data from mice exposed to intermittent hypoxia and mice reared for 12 months. We used microarrays to analyze the transcriptome of hippocampus from mice exposed to intermittent hypoxia or aged mice.

Publication Title

Treatment of intermittent hypoxia increases phosphorylated tau in the hippocampus via biological processes common to aging.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE28574
Transcriptome expressed in the mouse suprachiasmatic nucleus
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

This array set was used to identify the genes that are highly expressed in the mouse suprachiasmatic nucleus (SCN). Because pharmacological inhibition of Gai/o activity with pertussis toxin hampers intercellular synchronization and causes dampened rhythms of the entire SCN, we hypothesized that member(s) of the Regulator of G protein Signaling (RGS) family might contribute to synchronized cellular oscillations in the SCN. To test this hypothesis, we surveyed all known mouse Rgs genes for their expression by using GeneChip and selected the genes that are highly expressed in the SCN for further analysis.

Publication Title

Circadian regulation of intracellular G-protein signalling mediates intercellular synchrony and rhythmicity in the suprachiasmatic nucleus.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Treatment, Time

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accession-icon GSE25827
ERK5 Regulates Muscle Cell Fusion through Klf Transcription Factors
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

In skeletal muscle differentiation, muscle-specific genes are regulated by two groups of transcription factors, the MyoD and MEF2 families, which work together to drive the differentiation process. Here we show that ERK5 regulates muscle cell fusion through Klf transcription factors. The inhibition of ERK5 activity suppresses muscle cell fusion with minimal effects on the expression of MyoD, MEF2, and their target genes. Promoter analysis coupled to microarray assay reveals that Klf-binding motifs are highly enriched in the promoter regions of ERK5-dependent upregulated genes. Remarkably, Klf2 and Klf4 expression are also upregulated during differentiation in an ERK5-dependent manner, and knockdown of Klf2 or Klf4 specifically suppresses muscle cell fusion. Moreover, we show that the Sp1 transcription factor links ERK5 to Klf2/4, and that nephronectin, a Klf transcriptional target, is involved in muscle cell fusion. Therefore, an ERK5/Sp1/Klf module plays a key role in the fusion process during skeletal muscle differentiation.

Publication Title

ERK5 regulates muscle cell fusion through Klf transcription factors.

Sample Metadata Fields

Cell line, Time

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accession-icon GSE12637
AC61 Vector vs. pRb
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
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Description

This experiment is to identify genes that are regulated by pRb in AC61 cells. AC61 cells were derived from a C-cell adenocarcinoma developed in an Rb+/-N-ras-/- mouse.

Publication Title

Rb Regulates DNA damage response and cellular senescence through E2F-dependent suppression of N-ras isoprenylation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE17462
Expression data from Bmi1-overexpressing Ink4a-Arf-null hepatoblasts
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Forced expression of Bmi1 accelerated the self-renewal of hepatic stem/progenitor cells and eventually induced their transformation in an in vivo transplant model. The Ink4a/Arf locus, which encodes a cyclin-dependent kinase inhibitor, p16Ink4a, and a tumor suppressor, p19Arf, is a pivotal target of Bmi1. Therefore, it would be of importance to understand the contribution of the Ink4a/Arf locus to Bmi1 oncogenic functions in cancer and search for as-yet-unknown Bmi1 target genes other than Ink4a/Arf. We used microarrays to explore novel candidate downstream targets for Bmi1 in hepatic stem/progenitor cells

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE33808
Expression data from Ezh2-null leukemic cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
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Description

The polycomb group (PcG) proteins function in gene silencing through histone modifications. They form chromatin-associated multiprotein complexes, termed polycomb repressive complex (PRC) 1 and PRC2. These two complexes work in a coordinated manner in the maintenance of cellular memories through transcriptional repression of target genes. EZH2 is a catalytic component of PRC2 and trimethylates histone H3 at lysine 27 to transcriptionally repress the target genes. PcG proteins have been characterized as general regulators of stem cells, but recent works also unveiled their critical roles in cancer.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE45624
The FLS (Fatty liver Shionogi) mouse, liver with non-alcoholic steatohepatitis (NASH)
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

Comparison between livers of FLS mice and livers of DS (DD shionogi) mice

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE15581
Mouse primary megakaryocytes, wild type & NF-E2p45-deficient
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

To identify p45 target genes, we conducted gene expression profiling with p45-null megakaryocytes cultured from E14.5 fetal liver. Many genes encoding membrane proteins and enzymes related to platelet function, including Txas, Glycoprotein 6 (Gp6) and Selectin P (Selp), were repressed in the absence of p45. Considering the similar DNA binding specificity of p45 and Nrf2 in vitro, we expected p45 to activate cytoprotective genes that are established Nrf2 targets. However, the expression of numerous detoxifying enzymes and stress-responsive genes, including NAD(P)H:quinone oxidoreductase (Nqo1), were increased in the absence of p45.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE21754
Expression data from white adipose tissue of Perilipin A transgenic mice
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

Perilipin A (PeriA) exclusively locates on adipocyte lipid droplets and is essential for lipid storage and lipolysis. Adipocyte specific overexpression of PeriA caused resistance to diet-induced obesity and resulted in improved insulin sensitivity. In order to better understand the biological basis for this observed phenotype we performed DNA microarray analysis on white adipose tissue (WAT) from PeriA transgenic (Tg) and control wildtype (WT) mice.

Publication Title

Perilipin overexpression in white adipose tissue induces a brown fat-like phenotype.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE24928
Gene expression change induced by bisphenol A in mouse urogenital sinus
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon

Description

Bisphenol A (BPA), an endocrine-disrupting chemical (EDC), is a well-known, ubiquitous estrogenic chemical. To investigate the effects of fetal exposure to low-dose BPA on the development of the prostate, we first examined the alterations of in situ sex steroid hormonal environment in the mouse urogenital sinus (UGS).

Publication Title

Endocrine disrupter bisphenol A increases in situ estrogen production in the mouse urogenital sinus.

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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