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accession-icon GSE42867
Gene expression changes in subclones of a Burkitt lymphoma cell line with different patterns of EBV latent infection
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In this study we have investigated the gene expression profiles of three different types of subclone all generated by single cell cloning of the same parental EBV positive Burkitt lymphoma cell line Awia-BL. These included EBV negative clones which have lost the virus episome, EBV positive clones with a conventional Latency I form of infection and EBV positive clones with an atypical Wp-restricted form of infection.

Publication Title

Different patterns of Epstein-Barr virus latency in endemic Burkitt lymphoma (BL) lead to distinct variants within the BL-associated gene expression signature.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE29673
Toxicogenomic Study of Pentamethylchromanol (PMCol)
  • organism-icon Rattus norvegicus
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

The objective of this study is to determine the molecular mechanisms of PMCol-induced hapatotoxicity using microarray

Publication Title

Toxicogenomics and metabolomics of pentamethylchromanol (PMCol)-induced hepatotoxicity.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE79623
Gene expression analysis in the aorta from non-diabetic or STZ-induced diabetic apolipoprotein E deficient (ApoE-/-) mice fed with high fat diet in the presence or absence of PKC inhibitor, ruboxistaurin (RBX, or LY333531)
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We found that hyperglycemia and elevated fatty acids in diabetes could activate protein kinase C- isoforms and selectively induce insulin resistance via inhibiting vascular insulin signaling.

Publication Title

Insulin decreases atherosclerosis by inducing endothelin receptor B expression.

Sample Metadata Fields

Age, Specimen part, Disease, Disease stage, Treatment

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accession-icon E-MEXP-749
Transcription profiling by array of Arabidopsis after treatment with benzyladenine
  • organism-icon Arabidopsis thaliana
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis Genome Array (ag)

Description

10 day old seedlings were treated with 5uM of the cytokinin Benzyladenine(BA)or DMSO at 15min, 45min, 120min, 480min and 1440min

Publication Title

Expression profiling of cytokinin action in Arabidopsis.

Sample Metadata Fields

Age, Compound, Time

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accession-icon GSE7439
Escherichia coli strain 8624 and Escherichia coli strain VS94 with signaling molecules
  • organism-icon Escherichia coli
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

These E. coli strains were grown with various signaling molecules and the expression profiles were determined.

Publication Title

Global effects of the cell-to-cell signaling molecules autoinducer-2, autoinducer-3, and epinephrine in a luxS mutant of enterohemorrhagic Escherichia coli.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE18118
QseA regulation of virulence factors in EHEC
  • organism-icon Escherichia coli
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Enterohemorrhagic E. coli (EHEC) colonizes the large intestine and causes attaching and effacing lesions (AE). Most of the genes involved in the formation of AE lesions are encoded within a chromosomal pathogenicity island termed the Locus of Enterocyte Effacement (LEE). The LysR-like transcriptional factor QseA regulates the LEE by binding directly to the regulatory region of ler. Here, we performed transcriptome analyses comparing WT EHEC and the isogenic qseA mutant in order to elucidate the extent of QseAs role in gene regulation in EHEC. The following results compare genes that were up-regulated and down-regulated ! 2-fold in the qseA mutant strain compared to the WT strain. At mid-exponential growth, 222 genes were up-regulated and 1874 were downregulated. At late-exponential growth, a total of 55 genes were up-regulated and 605 genes were down-regulated. During mid-exponential growth, QseA represses its own transcription, whereas during late-logarithmic growth, QseA activates expression of the LEE genes as well as non-LEE encoded effector proteins. During both growth phases, several genes carried in O-islands, were activated by QseA, whereas genes involved in cell metabolism were repressed. We also performed electrophoretic mobility shift assays, competition experiments, and DNAseI footprints, and the results suggested that QseA directly binds both the ler proximal and distal promoters, its own promoter, as well as promoters of genes encoded in EHEC-specific O-islands. Additionally, we mapped the transcriptional start site of qseA, leading to the identification of two promoter sequences. Taken together, these results indicate that QseA acts as a global regulator in EHEC, coordinating expression of virulence genes.

Publication Title

The LysR-type regulator QseA regulates both characterized and putative virulence genes in enterohaemorrhagic Escherichia coli O157:H7.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP132608
Investigation of mRNA expression pattern by RAD21 knockdown in hematopoetic stem cells
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Elevated inflammation represents a hallmark of hematopoietic aging and leukemia development but mechanistically its impact on hematopoietic stem and progenitor cell (HSPC) maintenance remains incompletely understood. Here we identify Rad21/cohesin as a major component mediating inflammation-induced NF-kB signaling, which in turn limits self-renewal of HSPCs by induction of differentiation. Disruption of Rad21/cohesin diminishes inflammation-induced loss of self-renewal and induction of differentiation, but these effects are abrogated in NF-kB knockout (p50-/-) HSPCs. During aging, HSPCs exhibit an increased responsiveness to activate NF-kB signaling in response to inflammatory stimuli also resulting in activation of genes encoding for secreted cytokines. These cell intrinsic and extrinsic responses cooperatively enhance differentiation and loss of self-renewal of HSPCs resulting in increased selection of Rad21/cohesin deficient HSPCs exhibiting elevated self-renewal and myeloid skewed differentiation. Together, these results identify cohesin-mediated NF-kB signaling as a major axis connecting cell extrinsic increases in inflammation with the evolution of hallmark features HSC aging characterized by increases in self renewal and myeloid skewed differentiation aggravated by the concomitant selection of cohesin deficient HSPCs. Overall design: total samples: 12 (6 in vivo: 3 Rad21 knockdown, 3 control; 6 in vitro: 3 Rad21 knockdown, 3 control)

Publication Title

Cohesin-mediated NF-κB signaling limits hematopoietic stem cell self-renewal in aging and inflammation.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP102705
AKHR F1 heterozygous progeny of obese parents and controls, 10-11 days old adults
  • organism-icon Drosophila melanogaster
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Transgenerational effects of parental metabolic state have been shown, but the mechanism is still unclear. Here we present transcriptome sequencing data from AKHR heterozygous F1 progeny, either from obese maternal or paternal parents, compared to genetically matched heterozygous controls or to wild-type controls Overall design: 3 AKHR heterozygous samples descended from obese maternal parents, 3 AKHR heterozygous samples descended from obese paternal parents, 3 AKHR heterozygous samples descended from non-obese parents, and 3 wild-type controls, independent biological replicates and independent experimental replicates (1 set of samples from each experimental replicate)

Publication Title

Parental obesity leads to metabolic changes in the F2 generation in <i>Drosophila</i>.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE4179
A function for interleukin 2 in Foxp3-expressing regulatory T cells
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Regulatory T cells (Treg cells) expressing the forkhead family transcription factor Foxp3 are critical mediators of dominant immune tolerance to self. Most Treg cells constitutively express the high-affinity interleukin 2 (IL-2) receptor alpha-chain (CD25); however, the precise function of IL-2 in Treg cell biology has remained controversial. To directly assess the effect of IL-2 signaling on Treg cell development and function, we analyzed mice containing the Foxp3gfp knock-in allele that were genetically deficient in either IL-2 (Il2-/-) or CD25 (Il2ra-/-). We found that IL-2 signaling was dispensable for the induction of Foxp3 expression in thymocytes from these mice, which indicated that IL-2 signaling does not have a nonredundant function in the development of Treg cells. Unexpectedly, Il2-/- and Il2ra-/- Treg cells were fully able to suppress T cell proliferation in vitro. In contrast, Foxp3 was not expressed in thymocytes or peripheral T cells from Il2rg-/- mice. Gene expression analysis showed that IL-2 signaling was required for maintenance of the expression of genes involved in the regulation of cell growth and metabolism. Thus, IL-2 signaling seems to be critically required for maintaining the homeostasis and competitive fitness of Treg cells in vivo.

Publication Title

A function for interleukin 2 in Foxp3-expressing regulatory T cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12831
The role of qseE, qseF and qseG in the regulation of EHEC virulence
  • organism-icon Escherichia coli
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Escherichia coli 8624 and the isogenic mutants in qseE, qseF and qseG are compared to determine the role that each of the genes play in regulation of the transcriptome. These results are verified by qRT-PCR and reveal the important role of this three-component signaling system.

Publication Title

The two-component system QseEF and the membrane protein QseG link adrenergic and stress sensing to bacterial pathogenesis.

Sample Metadata Fields

No sample metadata fields

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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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