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accession-icon GSE35281
HIRA, a Conserved Histone Chaperone, Plays an Essential Role in Low-dose Stress Response via Transcriptional Stimulation in Fission Yeast
  • organism-icon Schizosaccharomyces pombe
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Cells that have been pre-exposed to mild stress (priming stress) acquire transient resistance to subsequent severe stress even under different combinations of stresses. This phenomenon is called cross-tolerance. Although it has been reported that cross-tolerance occurs in many organisms, the molecular basis is not clear yet. Here, we identified slm9+ as a responsible gene for the cross-tolerance in the fission yeast Schizosaccharomyces pombe. Slm9 is a homolog of mammalian HIRA histone chaperone. HIRA forms a conserved complex and gene disruption of other HIRA complex components, Hip1, Hip3, and Hip4, also yielded a cross-tolerance-defective phenotype, indicating that the fission yeast HIRA is involved in the cross-tolerance as a complex. We also revealed that Slm9 was recruited to the stress-responsive gene loci upon stress treatment in an Atf1-dependent manner. The expression of stress-responsive genes under stress conditions was compromised in HIRA disruptants. Consistent with this, Pol II recruitment and nucleosome eviction at these gene loci were impaired in slm9D cells. Furthermore, we found that the priming stress enhanced the expression of stress-responsive genes in wild-type cells that were exposed to the severe stress. These observations suggest that HIRA functions in stress response through transcriptional regulation.

Publication Title

HIRA, a conserved histone chaperone, plays an essential role in low-dose stress response via transcriptional stimulation in fission yeast.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE9884
Expression Profiling of Circulating Red Blood Cells and Non Red Blood Cells in the Chicken Embryo (E4 and E6)
  • organism-icon Gallus gallus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Chicken Genome Array (chicken)

Description

Blood was extracted from embryonic hearts at E4 and E6 and non-red blood was separated by density gradient centrifugation

Publication Title

Expression profiling of circulating non-red blood cells in embryonic blood.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP093260
RNA-sequencing of B cells in the absence of Moz or c-Myb
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Humoral responses of mice specifically deleted for Moz (a histone acetyltransferase) or c-Myb (a transcription factor) in B cells were aberrant. RNA-sequencing analysis was performed to assess gene expression differences compared to wild-type controls in germinal center B cells or plasmablasts. Overall design: Moz f/f Aicda1-Cre, Aicda1-Cre, Myb f/f Cd23-Cre, Mybf/f (no cre) mice were immunized with NP-KLH precipitated in alum and germinal center B cells were sort-purified. Secondary plasmablasts were sort-purified from immunized mice boosted with NP-KLH in PBS (Myb experiment). Two independent experiments were conducted.

Publication Title

Regulation of germinal center responses and B-cell memory by the chromatin modifier MOZ.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE101141
Amniotic fluid transcriptomics reflects novel disease mechanisms in fetuses with myelomeningocele
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To identify molecular pathophysiologic changes and novel disease mechanisms specific to myelomeningocele by analyzing AFS cfRNA in fetuses with open myelomeningocele.

Publication Title

Amniotic fluid transcriptomics reflects novel disease mechanisms in fetuses with myelomeningocele.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE31744
Comparison of Flk-1+/PDGFRa+(Flk-1PRa+(DP)) population from Etv2Het vs Etv2KO ES cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Screening for genes regulated by Etv2 within Flk-1+/PDGFRa+ ES derived mesoderm.Microarray analysis performed to screen for the candidate genes regulated by Etv2. TT2 ES cells differentiated on OP9 feeder cells were sorted using Flk-1 and PDGFRa antibodies.Gene expressions from these two populations were compared.

Publication Title

Etv2/ER71 induces vascular mesoderm from Flk1+PDGFRα+ primitive mesoderm.

Sample Metadata Fields

Cell line

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accession-icon GSE31743
Comparison of Flk-1+/Etv2- vs Flk-1+/Etv2+ populations
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Screening for genes up in Etv2+ cells within Flk-1+ ES derived mesoderm

Publication Title

Etv2/ER71 induces vascular mesoderm from Flk1+PDGFRα+ primitive mesoderm.

Sample Metadata Fields

Cell line

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accession-icon GSE114565
Expression data of C.pn treated foam cell
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

C.pn potentiated hyperlipidemia-induced inflammasome activity in cultured macrophages and in foam cells in atherosclerotic lesions of Ldlr/ mice. We discovered that C.pn-induced extracellular IL-1 triggers a negative feedback loop to inhibit GPR109a and ABCA1 expression and cholesterol efflux leading to accumulation of intracellular cholesterol and foam cell formation. Gpr109a and Abca1 were both upregulated in plaque lesions in Nlrp3/ mice in both hyperlipidemic and C.pn infection models.

Publication Title

Chlamydia pneumoniae Hijacks a Host Autoregulatory IL-1β Loop to Drive Foam Cell Formation and Accelerate Atherosclerosis.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP090980
A genetic screen identifies hypothalamic Fgf15/19 as a regulator of glucagon secretion
  • organism-icon Mus musculus
  • sample-icon 78 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The counterregulatory response to hypoglycemia, which restores normal blood glucose levels to ensure sufficient provision of glucose to the brain, is critical for survival. To discover underlying brain regulatory systems, we performed a genetic screen in recombinant inbred mice for quantitative trait loci (QTL) controlling glucagon secretion in response to neuroglucopenia. We identified a QTL on the distal part of chromosome 7 and combined this genetic information with transcriptomic analysis of hypothalami. This revealed Fgf15 as the strongest candidate to control the glucagon response. Fgf15 was found to be expressed by neurons of the dorsomedial hypothalamus and the perifornical area. Intracerebroventricular injection of FGF19, the human ortholog of Fgf15, reduced activation by neuroglucopenia of dorsal vagal complex neurons and of the parasympathetic nerve, leading to a lower glucagon secretion. These data show that Fgf15 in hypothalamic neurons is a regulator of vagal nerve activity in response to neuroglucopenia. Overall design: 36 BXD strains + 4 parental strains, 1 time point, basal condition without treatment

Publication Title

A Genetic Screen Identifies Hypothalamic Fgf15 as a Regulator of Glucagon Secretion.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE77559
MAFG is a transcriptional repressor of bile acid synthesis and metabolism
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

MAFG is a transcriptional repressor of bile acid synthesis and metabolism.

Sample Metadata Fields

Treatment

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accession-icon GSE77507
Differential gene expression following MafG overexpression
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Specific bile acids are potent signaling molecules that modulate metabolic pathways affecting lipid, glucose and bile acid homeostasis, and the microbiota. Bile acids are synthesized from cholesterol in the liver, and the key enzymes involved in bile acid synthesis (Cyp7a1, Cyp8b1) are regulated transcriptionally by the nuclear receptor FXR. We have identified an FXR-regulated pathway upstream of a transcriptional repressor that controls multiple bile acid metabolism genes. We identify MafG as an FXR target gene and show that hepatic MAFG overexpression represses genes of the bile acid synthetic pathway and modifies the biliary bile acid composition. In contrast, loss-of-function studies using MafG(+/-) mice causes de-repression of the same genes with concordant changes in biliary bile acid levels. Finally, we identify functional MafG response elements in bile acid metabolism genes using ChIP-seq analysis. Our studies identify a molecular mechanism for the complex feedback regulation of bile acid synthesis controlled by FXR

Publication Title

MAFG is a transcriptional repressor of bile acid synthesis and metabolism.

Sample Metadata Fields

Treatment

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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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