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accession-icon GSE19374
Expression data from mouse bone marrow derived macrophages
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Macrophages phagocytose bacteria. Certain pathogenic bacteria access and replicate within the cytosol of infected macrophages and induce changes in macrophage gene expression by triggering of innate immune receptors and/or the effects of bacterial virulence factors. We used microarray analysis to identify changes in macrophage gene expression following infection with Listeria monocytogenes.

Publication Title

Induction of IFN-alphabeta enables Listeria monocytogenes to suppress macrophage activation by IFN-gamma.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE64123
Human embryonic stem cell based neuro-developmental toxicity assay: response to valproic acid and carbamazepine exposure
  • organism-icon Homo sapiens
  • sample-icon 90 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Here we studied the effects of anticonvulsant drug exposure in a human embryonic stem cell (hESC) based neuro- developmental toxicity test (hESTn). During neural differentiation the cells were exposed, for either 1 or 7 days, to non-cytotoxic concentration ranges of valproic acid (VPA) or carbamazepine (CBZ), anti-epileptic drugs known to cause neurodevelopmental toxicity.

Publication Title

Gene Expression Regulation and Pathway Analysis After Valproic Acid and Carbamazepine Exposure in a Human Embryonic Stem Cell-Based Neurodevelopmental Toxicity Assay.

Sample Metadata Fields

Time

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accession-icon GSE55618
Toxicogenomic profiling in the whole zebrafish embryo after exposure to reference hepatotoxicants.
  • organism-icon Danio rerio
  • sample-icon 188 Downloadable Samples
  • Technology Badge Icon Affymetrix Genechip Zebrafish ST Genome Array 1.1 (zebgene11st)

Description

Zebrafish embryos have been proposed as an attractive alternative model system for hepatotoxicity testing.

Publication Title

A transcriptomics-based hepatotoxicity comparison between the zebrafish embryo and established human and rodent in vitro and in vivo models using cyclosporine A, amiodarone and acetaminophen.

Sample Metadata Fields

Compound

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accession-icon GSE18397
Expression profiling of NB4 cells after treatment with ATRA
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

In acute promyelocytic leukemia (APL), differentiation therapy with all-trans retinoic acid (ATRA)

Publication Title

Chemokine induction by all-trans retinoic acid and arsenic trioxide in acute promyelocytic leukemia: triggering the differentiation syndrome.

Sample Metadata Fields

Specimen part

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accession-icon SRP165285
RNA-Seq of WT and constitutively methylated mESCs
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconNextSeq 550

Description

WT J1 and 3B3L cells (in which Dnmt3B and Dnm3L are constitutively expressed from an exogenous construct) were cultured under both serum/LIF and 2i/LIF conditions. 3B3L cells do not show ground state-associated hypomethylation phenotype. This experiment sought to analyse the gene expression changes between the two conditions. Overall design: Three biological replicates per condition J1 serum, J1 2i, 3B3-3l serum, 3B3-3l 2i.

Publication Title

DNA Methylation Directs Polycomb-Dependent 3D Genome Re-organization in Naive Pluripotency.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon E-TABM-585
Transcription profiling by array of human lung cancer cells after treatment with dasatinib, imatinib, nilotinib or PD0325901
  • organism-icon Homo sapiens
  • sample-icon 111 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Human Genome U133A Array (hthgu133a)

Description

Cell Line: This experiment was designed to measure the transcriptional responses to four kinase inhibitors across a five-logarithm dose range. The A549 human lung cancer cell line was treated with dasatinib, imatinib or nilotinib (4 hours and 20 hours) or PD0325901 (4 hours). Treatments used a 12-point dose range (30 uM with 3-fold dilutions down to 0.17 nM; 0.5% DMSO vehicle for all treatments). Experimental design prevented row or column handling effects being confounded with dose effect.

Publication Title

Transcriptional profiling of the dose response: a more powerful approach for characterizing drug activities.

Sample Metadata Fields

Disease, Cell line, Compound, Time

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accession-icon E-TABM-450
Transcription profiling by array of human lung cancer cells after treatment with various inhibitors of LIMK1 and LIMK2
  • organism-icon Homo sapiens
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Human Genome U133A Array (hthgu133a), Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

To investigate an unknown mechanism of cytotoxicity, A549 human lung-cancer cells were treated with compounds from a series of inhibitors developed against the human LIM kinases LIMK1 and LIMK2. Compounds 1 and 2 inhibit LIM kinase activity in vitro and affect cell proliferation and survival in vivo. Compounds 3 and 4 inhibit LIM kinases but do not affect cell survival or proliferation. Compounds 5 and 6 affect proliferation and survival but do not inhibit LIM kinases. Nocodazole was included as a comparator because the compounds were known to affect microtubule stability. A treatment of 7 hours was used to examine events prior to apoptosis, while the dose levels captured both cytotoxicity and inhibition of LIMKs (Compounds 1 and 2), LIMK inhibition alone ( Compounds 3 and 4) or cytotoxicity alone (Compounds 5, 6, and Nocodazole).

Publication Title

Identification of a nonkinase target mediating cytotoxicity of novel kinase inhibitors.

Sample Metadata Fields

Cell line, Subject, Compound

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accession-icon SRP020625
Holo-TFIID controls the magnitude of a transcription burst and fine-tuning of transcription.
  • organism-icon Drosophila melanogaster
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

TFIID is a central player in activated transcription initiation. Recent evidence suggests that the role and composition of TFIID is more diverse than previously understood. To investigate the effects of changing the composition of TFIID in a simple system we depleted TAF1 from Drosophila cells and determined the consequences on metal induced transcription at an inducible gene, Metallothionein B (MtnB). We observe a marked increase in the levels of both the mature message and pre-mRNA in TAF1 depleted cells. Under conditions of continued metal exposure, we show that TAF1 depletion increases the magnitude of the initial transcription burst, but has no effect on the timing of that burst. We also show that TAF1 depletion causes delay in the shut-off of transcription upon removal of the stimulus. Thus TAFs are involved in both establishing an upper limit of transcription during induction and efficiently turning the gene off once the inducer is removed. Using genomewide nascent-seq we identify hundreds of genes that are controlled in a similar manner indicating that the findings at this inducible gene are likely generalizable to a large set of promoters. There is a long-standing appreciation for the importance of the spatial and temporal control of transcription. Here we uncover an important third dimension of control, the magnitude of the response. Our results show that the magnitude of the transcriptional response to the same signaling event, even at the same promoter, can vary greatly depending on the composition of the TFIID complex in the cell. Overall design: Nascent RNA was sequenced from replicate samples of Drosophila S2 cells treated with double-stranded RNA directed against E. coli LacI (Control) or against Drosophlia TAF1 (experimental). Reads per kilo-base per million (RPKM) was determined for each gene and the control and experimental samples were compared to determine the genes that were affected by the depletion of TAF1.

Publication Title

Holo-TFIID controls the magnitude of a transcription burst and fine-tuning of transcription.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE13131
Gene expression profiling of LNCaP and PC-3 prostate cancer cell lines
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

BACKGROUND. Human prostate cancer LNCaP and PC-3 cell lines have been extensively used as prostate cancer cell models to study prostate cancer progression and to develop therapeutic agents. Although LNCaP and PC-3 cells are generally assumed to represent early and late stages of prostate cancer development, respectively, there is limited information regarding comprehensive gene expression patterns between these two cells lines and relating these cells to prostate cancer progression based on their gene expression.

Publication Title

Unique patterns of molecular profiling between human prostate cancer LNCaP and PC-3 cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE75519
Gene microarray of sorted Vg9Vd2 subsets
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Analysis of gene expression at RNA level by 4 different cell sorted Vg9Vd2 subsets (Subset 1=CD28+CD27+, Subset2=CD28-CD27+, Subset 3=CD28-CD7-CD16-, Subset 4 = CD28-CD27-CD16+). Results highlight differences in RNA expression characterising these four cell populations into distinct phenotypic subsets with distinct functional potential

Publication Title

Heterogeneous yet stable Vδ2(+) T-cell profiles define distinct cytotoxic effector potentials in healthy human individuals.

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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