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accession-icon SRP074138
Human islets contain four distinct subtypes of ß cells
  • organism-icon Homo sapiens
  • sample-icon 31 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Illumina HiSeq 2500

Description

The transcriptomes of four subpopulations of beta cells isolated by FACS from five healthy human donors. Populations were defined using cell surface-labeling antibodies, avoiding the need for fixation. Overall design: There are 5 biological replicates of 4 different cell types. Each donor yielded all 4 subtypes.

Publication Title

Human islets contain four distinct subtypes of β cells.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP038989
mCasz1_conditional knockout
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The overall goal of our studies is to elucidate the cellular and molecular mechanism by which the transcription factor Casz1 functions in murine heart development. We established that Casz1 is expressed in myocardial progenitor cells beginning at E7.5 and in differentiated cardiomyocytes throughout development. We generated conditional Casz1 knockout mice to show that ablation of CASZ1 in Nkx2.5-positive cardiomyocytes leads to cardiac hypoplasia, ventricular septal defects and lethality by E13.5. To identify the pathways and networks by which Casz1 regulates cardiomyocyte development, we used RNA-Seq and identified genes involved in cell proliferation are upregulated in Casz1 mutants compared to wild-type littermates. We conclude that Casz1 is essential for cardiac development and has a pivotal role in regulating part of the cardiac transcriptional program. Overall design: 3 biological replicates of the two genotypes (Nkx2-5+/+,Casz1f/+ and Nkx2-5Cre/+,Casz1f/f) were used for RNA-seq to determine genes that are differentially expressed in the murine heart when Casz1 is mutated. Nkx2-5+/+,Casz1f/+ were used as wild-type controls for comparison.

Publication Title

Casz1 is required for cardiomyocyte G1-to-S phase progression during mammalian cardiac development.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE5680
Expression data for an eQTL experiment in rat eye
  • organism-icon Rattus norvegicus
  • sample-icon 120 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

We used expression quantitative trait locus mapping in the laboratory rat (Rattus norvegicus) to gain a broad perspective of gene regulation in the mammalian eye and to identify genetic variation relevant to human eye disease. Of >31,000 gene probes represented on an Affymetrix expression microarray, 18,976 exhibited sufficient signal for reliable analysis and at least 2-fold variation in expression among 120 F2 rats generated from an SR/JrHsd x SHRSP intercross. Genome-wide linkage analysis with 399 genetic markers revealed significant linkage with at least one marker for 1,300 probes (alpha = 0.001; estimated empirical false discovery rate = 2%). Both contiguous and noncontiguous loci were found to be important in regulating mammalian eye gene expression. We investigated one locus of each type in greater detail and identified putative transcription-altering variations in both cases. We found an inserted cREL binding sequence in the 5' flanking sequence of the Abca4 gene associated with an increased expression level of that gene, and we found a mutation of the gene encoding thyroid hormone receptor beta 2 associated with a decreased expression level of the gene encoding short-wave sensitive opsin (Opn1sw). In addition to these positional studies, we performed a pairwise analysis of gene expression to identify genes that are regulated in a coordinated manner and used this approach to validate two previously undescribed genes involved in the human disease Bardet-Biedl syndrome. These data and analytic approaches can be used to facilitate the discovery of additional genes and regulatory elements involved in human eye disease.

Publication Title

Regulation of gene expression in the mammalian eye and its relevance to eye disease.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE47681
trkB.T1 WT versus trkB.T1 KO expression data following spinal cord injury (SCI)
  • organism-icon Mus musculus
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We profiled spinal cord tissue at the site of a moderate contusion injury at the level of the thoracic spinal cord

Publication Title

TrkB.T1 contributes to neuropathic pain after spinal cord injury through regulation of cell cycle pathways.

Sample Metadata Fields

Age, Specimen part, Time

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accession-icon SRP131067
Roles of the Brca2 and Wapl complexes with Pds5 in sister chromatid cohesion, cohesin localization, and gene expression [RNA-seq]
  • organism-icon Drosophila melanogaster
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

RNA expression was measured by RNA-seq in Drosophila ML-DmBG3-c2 cells depleted for proteins involved in sister chromatid cohesion, and in developing third instar wing discs with or withough brca2 gene mutations Overall design: RNA expression in depleted cells was compared to mock treated cells and RNA expression in wing discs from brca2 mutant Drosophila was compared to expression in wing discs without brca2 mutations This series includes mock RNAi treated samples re-used from GSE100547.

Publication Title

Brca2, Pds5 and Wapl differentially control cohesin chromosome association and function.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE11611
Combined gene expression and QTL analysis of soybean quantitative resistance to Phytophthora sojae
  • organism-icon Glycine max
  • sample-icon 2522 Downloadable Samples
  • Technology Badge Icon Affymetrix Soybean Genome Array (soybean)

Description

To identify soybean genes and QTLs associated with quantitative resistance to infection by the oomycete pathogen Phytophthora sojae, we conducted a very large-scale microarray experiment using 2522 Affymetrix GeneChips. The experiment involved assaying a total of 298 soybean recombinant inbred lines together with internal checks.

Publication Title

Infection and genotype remodel the entire soybean transcriptome.

Sample Metadata Fields

Specimen part

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accession-icon GSE21834
Identification of the receptor tyrosine kinase AXL in triple negative breast cancer as a novel target for the human miR-34a microRNA
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Identification of the receptor tyrosine kinase AXL in breast cancer as a target for the human miR-34a microRNA.

Sample Metadata Fields

Cell line

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accession-icon GSE64920
Caspase-2-dependent tumor suppression does not depend on the scaffold protein Raidd
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The receptor-interacting protein-associated ICH-1/CED-3 homologous protein with a death domain (Raidd) functions as a dual adaptor protein due to its bipartite nature, and is therefore thought to be a constituent of different multiprotein complexes including the PIDDosome, where it connects the cell death-related protease, Caspase-2, with the p53-induced protein with a death domain 1 (Pidd1). As such, Raidd has been implicated in DNA-damage-induced apoptosis as well as in tumor suppression, the latter based on its role as a direct activator of Caspase-2, known to delay lymphomagenesis caused by overexpression of c-Myc or loss of ATM kinase. As loss of Caspase-2 leads to an acceleration of tumor onset in the E-Myc mouse model we set out to interrogate the role of Raidd in this process in more detail. Our data obtained analyzing E-Myc/Raidd-/- mice indicate that Raidd is unable to protect from c-MYC-driven lymphomagenesis. Similarly, we failed to observe an effect of Raidd-deficiency on thymic lymphomagenesis induced by y-irradiation or fibrosarcoma development driven by 3-methylcholanthrene. The role of Caspase-2 as a tumor suppressor can therefore be uncoupled from its ability to interact and auto-activate upon binding to Raidd. Further, we provide supportive evidence that the tumor suppressive role of Caspase-2 is related to maintaining genomic integrity and allowing efficient p53-mediated signaling. Overall, our findings suggest that Raidd, although described to be the key-adapter allowing activation of the tumor suppressor Caspase-2, fails to suppress tumorigenesis in vivo.

Publication Title

The tumor-modulatory effects of Caspase-2 and Pidd1 do not require the scaffold protein Raidd.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP110597
Polycomb Repressive Complex 1 regulates transcription of active genes [RNAseq]
  • organism-icon Drosophila melanogaster
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

RNA expression was measured using RNA-seq Overall design: RNA levels in Mock-treated control Drosophila cells were compared to RNA levels in cells RNAi depleted for Ph, Sce, and Pc

Publication Title

Polycomb repressive complex 1 modifies transcription of active genes.

Sample Metadata Fields

Subject

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accession-icon SRP110596
Polycomb Repressive Complex 1 regulates transcription of active genes [NTseq]
  • organism-icon Drosophila melanogaster
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

RNA nascent transcription was measured using NT-seq Overall design: RNA nascent transcript levels in Mock-treated control Drosophila cells were compared to those in cells RNAi depleted for Ph and Sce

Publication Title

Polycomb repressive complex 1 modifies transcription of active genes.

Sample Metadata Fields

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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