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accession-icon GSE60762
Expression data of osteoarthritic and healthy human labrum cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Osteoarthritic cartilage has largely been investigated, however supporting structures as the acetabular labrum are less investigated. In this studies we aimed to identify differences in gene expression between healthy and osteoarthritic labrum cells

Publication Title

Distinct dysregulation of the small leucine-rich repeat protein family in osteoarthritic acetabular labrum compared to articular cartilage.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE466
mRNA expression in regenerated mdx mouse skeletal muscle
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Despite over 3,000 articles published on dystrophin in the last 15 years, the reasons underlying the progression of the human disease, differential muscle involvement, and disparate phenotypes in different species are not understood. The present experiment employed a screen of 12,488 mRNAs in 16-wk-old mouse mdx muscle at a time when the skeletal muscle is avoiding severe dystrophic pathophysiology, despite the absence of a functional dystrophin protein. A number of transcripts whose levels differed between the mdx and human Duchenne muscular dystrophy were noted. A fourfold decrease in myostatin mRNA in the mdx muscle was noted. Differential upregulation of actin-related protein 2/3 (subunit 4), beta-thymosin, calponin, mast cell chymase, and guanidinoacetate methyltransferase mRNA in the more benign mdx was also observed. Transcripts for oxidative and glycolytic enzymes in mdx muscle were not downregulated. These discrepancies could provide candidates for salvage pathways that maintain skeletal muscle integrity in the absence of a functional dystrophin protein in mdx skeletal muscle.

Publication Title

Regenerated mdx mouse skeletal muscle shows differential mRNA expression.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE39676
Geminin represses mesendoderm cell fate acquisition in embryoid bodies
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Geminin is a small nucleoprotein that neuralizes ectoderm in the Xenopus embryo. Geminin promotes neural fate acquisition of mouse embryonic stem cells: Geminin knockdown during neural fate acquisition decreased expression of neural precursor cell markers (Pax6, Sox1), while increasing expression of Pitx2, Lefty1 and Cited2, genes involved in formation of the mouse node. Here we differentiated mouse embryonic stem cells into embryoid bodies to study Geminin's ability to repress primitive streak mesendoderm fate acquisition. We used microarrays to define the sets of genes that are regulated by Geminin during cell fate acquisition in embryoid bodies, using Dox-inducible Geminin knockdown or overexpression mouse embryonic stem cell lines.

Publication Title

Geminin restrains mesendodermal fate acquisition of embryonic stem cells and is associated with antagonism of Wnt signaling and enhanced polycomb-mediated repression.

Sample Metadata Fields

Specimen part

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accession-icon GSE25737
Geminin-regulated genes during neural fate acquisition of mouse embryonic stem cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Formation of the complex vertebrate nervous system begins when pluripotent cells of the early embryo are directed to acquire a neural fate. Although cell intrinsic controls play an important role in this process, the molecular nature of this regulation is not well defined. Here we assessed the role for Geminin, a nuclear protein expressed in embryonic cells, in neural fate acquisition from mouse embryonic stem (ES) cells. While Geminin knockdown does not affect the ability of ES cells to maintain or exit pluripotency, we found that it significantly impairs their ability to acquire a neural fate. Conversely, Geminin overexpression promotes neural gene expression, even in the presence of growth factor signaling that antagonizes neural transcriptional responses. These data demonstrate that Geminins activity contributes to mammalian neural cell fate acquisition. We investigated the mechanistic basis of this phenomenon and found that Geminin maintains a hyperacetylated and open chromatin conformation at neural genes. Interestingly, recombinant Geminin protein also rapidly alters chromatin acetylation and accessibility even when Geminin is combined with nuclear extract and chromatin in vitro. These findings define a novel activity for Geminin in regulation of chromatin structure. Together, these data support a role for Geminin as a cell intrinsic regulator of neural fate acquisition that promotes expression of neural genes by regulating chromatin accessibility and histone acetylation.

Publication Title

Geminin promotes neural fate acquisition of embryonic stem cells by maintaining chromatin in an accessible and hyperacetylated state.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP113305
Functional and genomic characterization of a xenograft model system for the study of metastasis in triple-negative breast cancer.
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1500

Description

To define the molecular regulators of metastasis of triple-negative breast cancer, we conducted a rigorous characterization of four isogenic populations of MDA-MB-231 human triple-negative breast cancer cells that display a range of intrinsic spontaneous metastatic capacities in immuno-deficient mice, from non-metastatic to highly metastatic to lung, liver, spleen and spine. PAT-Seq gene expression profiling of primary tumor cells identified the fibroblast growth factor homologous factor, FGF13, as a candidate metastatic virulence gene highly upregulated in aggressively metastatic MDA-MB-231HM tumors. Overall design: Gene expression analysis from PAT-Seq of 4 increasingly metastatic breast cancer xenograft tumours

Publication Title

Functional and genomic characterisation of a xenograft model system for the study of metastasis in triple-negative breast cancer.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE8021
Expression data from human donor lung biopsies
  • organism-icon Homo sapiens
  • sample-icon 50 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Expression profile of human donor lungs that have developed primary graft dysfunction (PGD) after lung transplantation and those that have not.

Publication Title

Expression profiling of human donor lungs to understand primary graft dysfunction after lung transplantation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE7257
Laser capture-microarray analysis of Lim1 mutant kidney development.
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The Lim1 gene has essential functions during several stages of kidney development. In particular, a tissue specific knockout in the early metanephric mesenchyme results in the formation of the earliest nephron precursor, the renal vesicle, but failure of this structure to progress to the next stage, the comma shaped body. To better understand the molecular nature of this developmental arrest we used a laser capture microdissection-microarray strategy to examine the perturbed gene expression pattern of the mutant renal vesicles. Among the genes found differently expressed were Chrdl2, an inhibitor of BMP signaling, the pro-apoptotic factor Bmf, as well as myob5, an atypical myosin which modulates chemokine and transferring signaling, and pdgfr1, which is important in epithelial folding. Of particular interest, the microarray data indicated that the Dkk1 gene, which encodes an inhibitor of Wnt signaling, was downregulated nine fold in mutants. This was confirmed by in situ hybridizations. It is interesting to note that Lim1 and Dkk1 mutant mice have striking similarities in phenotype. These results suggest that the Dkk1 gene might be a key downstream effector of Lim1 function.

Publication Title

Laser capture-microarray analysis of Lim1 mutant kidney development.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE3808
Complete embryonic metanephric kidney analysis of wild type and Hoxa11, Hoxd11 null targeted mice
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Complete (whole) embryonic kidneys were dissected from wild type and Hoxa11, Hoxd11 compound null embryons throughout development. Targets from two biological replicates of each were generated and the expression profiles were determined using Affymetrix MOE430A and MOE430B arrays. Comparisons between normal and mutant and comparisons of development samples identified global patterns of gene regulation in kidney development

Publication Title

Comprehensive microarray analysis of Hoxa11/Hoxd11 mutant kidney development.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE3822
Complete embryonic E11.5 metanephric kidney analysis of wild type and Hoxa11, Hoxd11 null targeted mice
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

E11.5 metanephric mesenchyme and ureteric bud were dissected from the E11.5 kidney rudiment using fine manual microdissection (ureteric bud only) or both fine manual microdissection and laser capture microdissection (metanephric mesenchyme) to define the gene expression profiles of these structures. Additionally, HoxA11, HoxD11 compound null E11.5 metanephric mesenchyme was obtained through laser capture microdissection allowing analysis of possible Hox targets in kidney development. Targets from multiple biological replicates of each were generated and the expression profiles were determined using Affymetrix MOE430_v2 arrays.

Publication Title

Comprehensive microarray analysis of Hoxa11/Hoxd11 mutant kidney development.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE29589
Comparison of root transcriptomes in Arabidopsis thaliana plants supplied with different forms of inorganic nitrogen
  • organism-icon Arabidopsis thaliana
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Plants aquire nitrogen from the soil, most commonly in the form of either nitrate or ammonium. Unlike ammonium, nitrate must be reduced (with NADH and ferredoxin as electron donors) prior to assimilation. Thus, nitrate nutrition imposes a substantially greater energetic cost than ammonium nutrition. Our goal was to compare the transcriptomes of nitrate-supplied and ammonium-supplied plants, with a particular interest in characterizing the differences in redox metabolism elicited by different forms of inorganic nitrogen.

Publication Title

Distinct signalling pathways and transcriptome response signatures differentiate ammonium- and nitrate-supplied plants.

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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