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accession-icon GSE13377
Enriched genes in the primary mouth of Xenopus laevis
  • organism-icon Xenopus laevis
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome Array (xenopuslaevis)

Description

Identification of genes enriched in the presumptive primary mouth. Dissected tissues from the primary mouth anlage and two other anterior regions for comparison, the anterior dorsal and ventral plus cement gland.

Publication Title

The Wnt antagonists Frzb-1 and Crescent locally regulate basement membrane dissolution in the developing primary mouth.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE3334
Genomic Profiling of Mixer and Sox17beta Targets During Xenopus Endoderm Development
  • organism-icon Xenopus laevis
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome Array (xenopuslaevis)

Description

The transcription factors Mixer and Sox17beta have well characterized roles in endoderm specification during Xenopus embryogenesis. In order to more thoroughly understand the mechanisms by which these endodermal regulators act, we expressed Mixer and Sox17beta in nave ectodermal tissue and, using oligonucleotide-based microarrays, compared their genomic transcriptional profile to that of unaffected tissue. Using this novel approach, we identified 71 transcripts that are upregulated by Mixer or Sox17beta, 63 of which have previously uncharacterized roles in endoderm development. Furthermore, an in situ hybridization screen using antisense probes for several of these clones identified six targets of Mixer and/or Sox17beta that are expressed in the endoderm during gastrula stages, providing new and regional markers of the endoderm. Our results contribute further insight into the functions of Mixer and Sox17beta and bring us closer to understanding at the molecular level the pathways that regulate endoderm development.

Publication Title

Genomic profiling of mixer and Sox17beta targets during Xenopus endoderm development.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE9590
Saccharomyces cerevisiae TPP 2-oxo acid decarboxylases
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

The irreversible decarboxylation step, which commits 2-oxo acids to the Ehrlich pathway, was initially attributed to pyruvate decarboxylase. However, the yeast genome was shown to harbour no fewer than 5 genes that show sequence similarity with thiamine-diphosphate dependent decarboxylase genes. Three of these (PDC1, PDC5 and PDC6) encode pyruvate decarboxylases { while ARO10 and THI3 represent alternative candidates for Ehrlich-pathway decarboxylases.

Publication Title

The Ehrlich pathway for fusel alcohol production: a century of research on Saccharomyces cerevisiae metabolism.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE51075
Transcriptional responses of murine macrophages to the adenylate cyclase toxin of Bordetella pertussis
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Three different recombinant forms of CyaA were used to investigate transcriptional responses of murine bone marrow-derived macrophages (BMDMs) using Affymetrix Mouse Genome Genechips. These forms were enzymically active, invasive CyaA, nonenzymically active, invasive CyaA (CyaA*) and non-enzymically active, non-invasive CyaA (proCyaA*). BMMs, treated with 20 ng/ml of CyaA for 24 h, showed over 1000 significant changes in gene transcription compared with control cells. CyaA caused an increase in transcription of many inflammatory genes and genes associated with various signalling cascades such as those involved in cyclic AMP-dependent protein kinase A signalling. Most strikingly, CyaA caused down-regulation of numerous genes involved in cell proliferation. CyaA* at 20 ng/ml significantly up-regulated the transcription of only twelve genes after 24 h whereas proCyaA* at this concentration significantly increased the transcription of only two genes.

Publication Title

Transcriptional responses of murine macrophages to the adenylate cyclase toxin of Bordetella pertussis.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

View Samples
accession-icon SRP126516
Transcriptome response of human skeletal muscle to divergent exercise stimuli
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

While acute aerobic and resistance exercise stimulate a number of shared genes, each exercsie mode stimlutes a number of uniquely responsive genes, thus highlighting that different forms of exercise facilitate distinct molecular responses in skeletal muscle. Overall design: Randomized, counter-balanced, cross-over design (n=6) in which subjects performed an acute bout aerobic and resistance exercise separated by ~1 week.

Publication Title

Transcriptome response of human skeletal muscle to divergent exercise stimuli.

Sample Metadata Fields

Sex, Subject, Time

View Samples
accession-icon GSE18795
Expression data from zebrafish embryos homozygous mutant for the cohesin subunit Rad21
  • organism-icon Danio rerio
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Rad21 is a subunit of cohesin. The main function of cohesin is to hold replicated chromosomes together until cells divide, but it also plays a role in gene expression. To find out which genes might be regulated by cohesin, a study was conducted to look for global changes in gene expression in zebrafish embryos lacking cohesin component Rad21.

Publication Title

Positive regulation of c-Myc by cohesin is direct, and evolutionarily conserved.

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon GSE46863
Clinical symptoms of right ventricular failure in experimental chronic pressure load are associated with progressive diastolic dysfunction
  • organism-icon Rattus norvegicus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.1 ST Array (ragene11st)

Description

Right ventricular failure (RVF) due to pressure load is a major cause of death in congenital heart diseases and pulmonary hypertension. The mechanisms of RVF are yet unknown. Research is hampered by the lack of a good RVF model. Our aim was to study the pathophysiology of RVF in a rat model of chronic pressure load.

Publication Title

Clinical symptoms of right ventricular failure in experimental chronic pressure load are associated with progressive diastolic dysfunction.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE9975
newly transcribed RNA (nt-RNA) for IFN alpha and gamma time course
  • organism-icon Mus musculus
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Expression data from NIH-3T3 cells treated with mock, 100 U/ml IFN alpha or 100 U/ml gamma for 1 or 3h on nt-RNA labeled for 30-60 min at different times of interferon treatment

Publication Title

High-resolution gene expression profiling for simultaneous kinetic parameter analysis of RNA synthesis and decay.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE9977
Expression data from NIH-3T3 cells treated with mock, 100 U/ml IFN alpha or 100 U/ml gamma for 1or 3h
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Differential gene expression caused by 1h and 3h of IFN alpha or gamma treatment was analyzed in total cellular RNA of NIH-3T3 cells compared to mock

Publication Title

High-resolution gene expression profiling for simultaneous kinetic parameter analysis of RNA synthesis and decay.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP113307
Loss of Apela peptide in mice causes low penetrance embryonic lethality and defects in early mesodermal derivatives
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Apela (also referred to as Elabela, Ende and Toddler) is a small signaling peptide that activates the G protein-coupled receptor Aplnr. We used CRISPR/Cas9 to generate a null, reporter-expressing allele, in order to study the role of Apela in the developing mouse embryo. We found that loss of Apela results in low penetrance cardiovascular defects that manifest after the onset of circulation. Targeted Apela null alleles exhibited different transcriptional activity depending on the presence or absence of a Neomycin selection cassette. These are referred to as Apela KO NEO-IN and Apela KO NEO-OUT strains, respectively. Despite subtle phenotypic characteristics that were unique to the NEO-OUT mutants, both Apela null strains shared the same variable expressivity of cardiovascular defects and the same penetrance of embryonic lethality. To investigate the earliest regulatory events leading to physical abnormalities in Apela mutants, we performed RNA-Seq on whole stage-matched and morphologically normal E7.5 embryos (3 wild-type, 6 Apela KO NEO-IN, and 6 Apela KO NEO-OUT individuals). We chose this stage because Apela is initially expressed in the embryo at late gastrulation, shortly after the emergence of extraembryonic mesoderm progenitors. Since modification of the Apela locus may influence the expression of neighboring genes, we examined the expression of upstream and downstream sequences and found no significant difference in their expression. Downregulated genes of interest included several mitochondrial genes, Ceacam2, Ulk4, and Mov10l1. Upregulated genes included the vascular endothelial growth factor Vegfc. Principal component analysis identified outliers (KO1 and KO9), both of which expressed lower levels of mesoderm markers. KO9 was further characterized by aberrant upregulation of erythroid and myeloid markers. This finding was confirmed in our study by qRT-PCR analysis of additional Apela null individuals. Overall design: 15 individual embryos were analyzed at E7.5. Embryos were stage-matched according to morphological landmarks. Control samples were wild-type (n=3), and Apela KO samples were null embryos from the NEO-IN (n=6, ‘KO1-6’) and NEO-OUT (n=6, ‘KO7-12) mutant strains. Whole embryos (including embryonic and extraembryonic tissues) were used for the analysis. Apela KO samples were isolated from homozygous KO intercrosses and therefore did not require genotyping.

Publication Title

Loss of Apela Peptide in Mice Causes Low Penetrance Embryonic Lethality and Defects in Early Mesodermal Derivatives.

Sample Metadata Fields

Specimen part, Cell line, Subject

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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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