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accession-icon GSE21679
Gene signatures in wound tissue as evidenced by molecular profiling in the chicken embryo model
  • organism-icon Gallus gallus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Chicken Genome Array (chicken)

Description

Modern functional genomic approaches may help to better understand the molecular events involved in tissue morphogenesis and to identify molecular signatures and pathways. We have recently applied transcriptomic profiling to evidence molecular signatures in the development of the normal chicken chorioallantoic membrane and in tumor engrafted on the CAM. We have now extended our studies by performing a transcriptome analysis in the wound model of the chicken CAM which is another relevant model of tissue morphogenesis. To induce granulation tissue formation, we performed wounding of the chicken CAM and compared gene expression to normal CAM at the same stage of development. Matched control samples from the same individual were used. We observed a total of 282 genes up-regulated and 44 genes downregulated assuming a false-discovery rate at 5 % and a fold change > 2. Furthermore, bioinformatics analysis lead to the identification of several categories that are associated to organismal injury, tissue morphology, cellular movement, inflammatory disease, development and immune system. Endothelial cell data filtering leads to the identification of several new genes with an endothelial cell signature. In summary, the chick chorioallantoic wound model allows the identification of gene signatures involved in granulation tissue formation and neoangiogenesis. This may constitute a fertile ground for further studies.

Publication Title

Gene signatures in wound tissue as evidenced by molecular profiling in the chick embryo model.

Sample Metadata Fields

Specimen part

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accession-icon E-MEXP-1310
Transcription profiling of Arabidopsis seedlings treated with NAE(12:0)
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Transcript profiling and gene expression studies in NAE-treated seedlings: Seeds were germinated and seedlings maintained for 4 d in liquid MS media supplemented with 35 uM NAE(12:0)(N-lauroylethanolamine) prior to RNA isolation.

Publication Title

N-Acylethanolamine metabolism interacts with abscisic acid signaling in Arabidopsis thaliana seedlings.

Sample Metadata Fields

Age, Specimen part, Compound

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accession-icon SRP012170
miR-155 promotes Th17 development by targeting Jarid2
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Genome-wide analysis was performed on microRNA 155+/+ and -/- Th17 cells to determine the differentially expressed transcripts that are regulated by miR-155. We found that Jarid2 was differentially expressed in absence of miR-155 and highlight the mechanism for the silencing of IL-22 by Jarid2 and PRC2 in miR-155-/- Th17 cells. Overall design: Comparison of transcriptome of Th17 cells in presence or absence of microRNA 155

Publication Title

miR-155 activates cytokine gene expression in Th17 cells by regulating the DNA-binding protein Jarid2 to relieve polycomb-mediated repression.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP052998
Physical and functional CSL-p53 interactions underlie control of cancer stromal cell evolution [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

Senescence of stromal fibroblasts has been linked to establishment of cancer associated fibroblasts (CAF) and aging-associated increase of tumors. However, in clinically occurring carcinomas, density and proliferation of CAFs are frequently increased rather than decreased. We previously showed that genetic deletion or down-modulation of the canonical Notch effector CSL/RBP-J? in skin dermal fibroblasts is sufficient for CAF activation with consequent development of multifocal keratinocyte tumors. We now show that CSL deletion or knockdown induces senescence of primary fibroblasts derived from dermis, oral mucosa, breast and lung. CSL functions in these cells as a constitutive direct repressor of multiple senescence- and CAF-effector genes. At the same time, it physically interacts with p53, repressing its activity, and p53 activation provides a failsafe mechanism against compromised CSL function. Concomitant loss of CSL and p53 overcomes fibroblast senescence, enhances expression of CAF effector genes and, in vivo, promotes tumour and stromal cell expansion. Together, the findings support a CAF activation/stromal evolution model under convergent CSL/p53 control. Overall design: Human Dermal Fibroblasts were transfected with two different siRNA against CSL in parallel with a control siRNA. Total RNA was extracted 3 days post-transfection, followed by RNA-Seq analysis.

Publication Title

Combined CSL and p53 downregulation promotes cancer-associated fibroblast activation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE59847
Global changes in gene expression in human dermal fibroblasts after CSL silencing
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Senescence of stromal fibroblasts has been linked to establishment of cancer associated fibroblasts (CAF) and aging-associated increase of tumors. However, in clinically occurring carcinomas, density and proliferation of CAFs are frequently increased rather than decreased. We previously showed that genetic deletion or down-modulation of the canonical Notch effector CSL/RBP-J-kappa in skin dermal fibroblasts is sufficient for CAF activation with consequent development of multifocal keratinocyte tumors. We now show that CSL deletion or knockdown induces senescence of primary fibroblasts derived from dermis, oral mucosa, breast and lung. CSL functions in these cells as a constitutive direct repressor of multiple senescence- and CAF-effector genes. At the same time, it physically interacts with p53, repressing its activity, with p53 activation providing a failsafe mechanism against compromised CSL function. Concomitant loss of CSL and p53 overcomes fibroblasts senescence, enhances CAF effector gene expression and, in vivo, promotes stromal and cancer cell expansion. Together, these findings support a CAF activation/stromal evolution model under convergent CSL/p53 control.

Publication Title

Combined CSL and p53 downregulation promotes cancer-associated fibroblast activation.

Sample Metadata Fields

Specimen part

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accession-icon SRP187302
Slow transcriptional elongation causes embryonic lethality and perturbs kinetic coupling of long neural genes [4sURDB-Seq]
  • organism-icon Mus musculus
  • sample-icon 41 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

The rate of RNA Polymerase II (RNAPII) elongation has an important role in the control of Alternative splicing (AS); however, the in vivo consequences of an altered elongation rate are unknown. Here, we generated mouse embryonic stem cells (ESCs) knocked-in for a slow elongating form of RNAPII. We show that a reduced transcriptional elongation rate results in early embryonic lethality in mice and impairs the differentiation of ESCs into the neural lineage. This is accompanied by changes in splicing and in gene expression in ESCs and along the pathway of neuronal differentiation. In particular, we found a crucial role for RNAPII elongation rate in transcription and splicing of long neuronal genes involved in synapse signaling. The impact of the kinetic coupling of RNAPII elongation rate with AS is more predominant in ESC-differentiated neurons than in pluripotent cells. Our results demonstrate the requirement for an appropriate transcriptional elongation rate to ensure proper gene expression and to regulate AS during development. Overall design: 4sURDB-Seq mouse wt and homozygous Polr2a[R749H] mutant embryonic stem cells in triplicates.

Publication Title

A slow transcription rate causes embryonic lethality and perturbs kinetic coupling of neuronal genes.

Sample Metadata Fields

Treatment, Subject

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accession-icon GSE56670
Expression data from SDH-disabled GIST
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Pediatric GIST commonly harbors a disabled succinate dehydrogenase complex (SDH), which yields tumors with highly conserved genomes but characteristic epigenomic signatures. Mysteriously, nearly half of such SDH-deficient GIST, including tumors from Carney Triad patients, lack identifiable mutations in SDH component genes and genes required for complex assembly (SDHA, SDHB, SDHC, SDHD, SDHAF, termed SDHx). Genomic sequencing coupled with DNA methylation and transcriptional profiling have exposed SDHC promoter-specific CpG island epimutation and concomitant gene silencing in the majority of SDHx-WT GIST.

Publication Title

Recurrent epimutation of SDHC in gastrointestinal stromal tumors.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE40444
Stabilization of OCT4 synthetic mRNA in adult human skin cells using small molecules
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The OCT4 transcription factor is involved in many cellular processes, including development, reprogramming, maintaining pluripotency and differentiation. Synthetic OCT4 mRNA was recently used (in conjunction with other reprogramming factors) to generate human induced pluripotent stem cells. Here, we discovered that BAY 11-7082 (BAY11) could significantly increase the expression of OCT4 following transfection of synthetic mRNA (synRNA) into adult human skin cells. Importantly, the increased levels of OCT4 resulted in significantly increased expression of genes downstream of OCT4, including the previously identified SPP1, DUSP4 and GADD45G. We also identified a novel OCT4 downstream target gene SLC16A9 which demonstrated significantly increased expression following elevation of OCT4 levels. This small molecule-based stabilization of synthetic mRNA expression may have multiple applications for future cell-based research and therapeutics.

Publication Title

BAY11 enhances OCT4 synthetic mRNA expression in adult human skin cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE19495
Global Gene Expression of Human Hepatoma Cells After Amino Acid Limitation
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

1507 known genes have been identified differentially regulated during HisOH treatment by more than 2 fold. This includes 250 down-regulated genes and 1257 up-regulated genes.

Publication Title

Expression profiling after activation of amino acid deprivation response in HepG2 human hepatoma cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE50091
Expression data from late-luteal bovine endometrium
  • organism-icon Bos taurus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Bovine Genome Array (bovine)

Description

In both beef and dairy cattle, the majority of embryo loss occurs in the first 14-16 days following insemination. During this period, the embryo is completely dependent on its maternal uterine environment for development, growth and ultimately survival, therefore an optimum uterine environment is critical to embryo survival.

Publication Title

Endometrial gene expression in high- and low-fertility heifers in the late luteal phase of the estrous cycle and a comparison with midluteal gene expression.

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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