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accession-icon GSE52350
Systems analysis of transcriptional data provides insights into muscle's biological response to botulinum toxin-A (BoNT-A)
  • organism-icon Rattus norvegicus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Introduction:The purpose of this study is to provide athe first global transcriptomic profiling and systems analysis of BoNT-A treated muscle over a one year period. Microarray analysis was performed on rat TA muscle from 4 groups (n=4/group) at 1,4, 12 and 52 weeks after BoNT-A injection and saline injected rats at 12 weeks as control. Fold changes were computed at each time point with respect to control. Results: Dramatic transcriptional adaptation occurs at 1 week with a paradoxical increase in expression of slow and immature isoforms; increased expression of genes in competing pathways of repair and atrophy; impaired mitochondrial biogenesis and increased metal ion imbalance. ECM adaptations occurred at 4weeks to the basal lamina and fibrillar ECM. The muscle transcriptome returned to the unperturbed state 12 weeks post-injection. Conclusion: Transcriptional adaptations resemble denervated muscle albeit some differences. Overall gene expression, across time, correlates with the generally accepted BoNT-A time course.

Publication Title

Systems analysis of transcriptional data provides insights into muscle's biological response to botulinum toxin.

Sample Metadata Fields

Specimen part

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accession-icon SRP059754
Signaling through MyD88 in bone marrow-derived cells promotes gastric tumorigenesis by inducing the TLR2/CD14 pathway in tumor cells
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Gan mice express Wnt1, Ptgs2, and Ptges, which develop inflammation-associated gastric tumors (Oshima et al, Gastroenterology 131: 1086, 2006). We examined the role of MyD88 in tumorigenesis by construction of Myd88-/- Gan mice and bone marrow transplantation into Gan mice from Myd88-/- mice. Overall design: Total RNA was prepared from wild-type normal glandular stomach (n=3: WT 1–WT 3), B6 C2mE mice (n=3: C2mE 1–C2mE 3), B6 Gan mice (n=3: Gan1–Gan3), B6 Gan MyD88-/- mice (n=3: Gan 1 (MyD88-/-)–Gan 3 (MyD88-/-)), and B6 bone marrow transplanted Gan mice from Myd88-/- mice (n=3: BMT-Gan 1 (from MyD88-/-)–BMT-Gan 3 (from MyD88-/-)). We used Illumina HiSeq 2000, and examined expression profiles.

Publication Title

NF-κB-induced NOX1 activation promotes gastric tumorigenesis through the expansion of SOX2-positive epithelial cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP134098
mRNA sequence Analysis of Apocynin treated MKN45
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Noxo1, a component of NADPH oxidase 1 (NOX1) complex, is upregulated in gastric cancer cells in a inflammation-dependent manner, and plays an important role in tumorigenesis (Oncogene, 33: 3820, 2014). To examine the mechanism of NOX1/ROS signaling in tumorigenesis, MKN45 gastric cancer cells were treated with apocynin, an inhibitor for NOX, and their gene expression was examined by RNA sequencing. Based on expression data, Sox2 was shown to be suppressed by apocynin, suggesting a role of Sox2 in a inflammation-associated gastric tumorigenesis. Overall design: Total mRNA expression profiles of Apocynin administrated MKN45 in 2 trials.

Publication Title

NF-κB-induced NOX1 activation promotes gastric tumorigenesis through the expansion of SOX2-positive epithelial cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon GSE18913
siRNA-mediated Egr-3 knockdown in VEGF-treated HUVEC
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Analysis of umbilical vein endothelial cells (HUVEC) treated with Egr-3 siRNA under the VEGF treatment for 0,1, and 4 h. Egr-3, a member of early growth response family, is immediately and dramatically induced by VEGF in HUVEC, which regulates expression of many genes related to endothelial activation.

Publication Title

Vascular endothelial growth factor activation of endothelial cells is mediated by early growth response-3.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE141650
Fibrosis growth factor 23 is a promoting factor for cardiac fibrosis in the presence of transforming growth factor-β1
  • organism-icon Rattus norvegicus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

We demonstrated that, four weeks after the pulmonary artery banding (PAB) operation, rats could be divided into two groups: an F+ group in which the fibrotic area occupied more than 6.5% of the whole area of the heart tissues, and an F- group in which the fibrotic area occupied less than 6.5% of this area.

Publication Title

Fibrosis growth factor 23 is a promoting factor for cardiac fibrosis in the presence of transforming growth factor-β1.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE7623
24 h-fasting effects on the brown and white adipose tissue and liver
  • organism-icon Rattus norvegicus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

The functional balance between brown adipose tissue (BAT) and white adipose tissue (WAT) is important for metabolic homeostasis. We compared the effects of fasting on the gene expression profiles in BAT, WAT and liver, using DNA microarray analysis. Tissues were obtained from rats that had been fed or fasted for 24 h. Taking the false discovery rate (FDR) into account, we extracted the top 1,000 genes that were expressed differentially between fed and fasted rats. In all three tissues, Gene Ontology analysis revealed marked changes in the expression of metabolism category genes and a hypergeometric test demonstrated that within this category, lipid and protein biosynthesis-related genes were down-regulated. These findings indicate simultaneous down-regulation of genes involved in energy-consuming pathways in the BAT, WAT and liver of fasted rats. In the BAT of fasted rats, there was marked up-regulation of genes in the protein ubiquitination category, suggesting that the ubiquitin-proteasome system is involved in saving energy as an adaptation to food shortage.

Publication Title

Up-regulation of genes related to the ubiquitin-proteasome system in the brown adipose tissue of 24-h-fasted rats.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE109696
ERG and FLI1 in endothelial cells
  • organism-icon Homo sapiens
  • sample-icon 8 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

Downregulation of ERG and FLI1 expression in endothelial cells triggers endothelial-to-mesenchymal transition.

Sample Metadata Fields

Specimen part

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accession-icon GSE40500
Expression data from endthelial cells in ductus arteriosus and aorta in rat fetuses or neonates
  • organism-icon Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Endothelial cells (Ecs) lining the blood vessels have been known to have a variety of functions and play a central role in homeostasis of the circulatory system.

Publication Title

Transcription profiles of endothelial cells in the rat ductus arteriosus during a perinatal period.

Sample Metadata Fields

Specimen part

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accession-icon GSE17112
Visualization of cancer initiating cell in the vascular niche utilized with transcriptional activity of PSF1
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Identification of cancer stem/initiating cells (CSCs/CICs) by a specific marker is useful for diagnosis and therapy of cancer. We have determined that PSF1 which plays a role in DNA replication in lower species is strongly expressed in wide range of normal stem cell population. Here, utilizing the transcriptional activity of PSF1 promoter in tumor cell xenograft model, we show that PSF1high cancer cells display malignant features including high proliferating activity, serial transplantation potential, and metastatic ability those are used for criteria of CSCs/CICs. PSF1high cancer cells localize in perivascular region and genetically display ES cell like signature. Silencing of PSF1 by RNAi inhibited growth of cancer cells mediated by disruption of DNA synthesis and chromosomal segregation. These suggested that PSF1 is a possible maker and a molecular target of CSCs/CICs.

Publication Title

PSF1, a DNA replication factor expressed widely in stem and progenitor cells, drives tumorigenic and metastatic properties.

Sample Metadata Fields

Cell line

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accession-icon GSE109662
Expression data in HUVECs treated with siERG, siFLI1, or both
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Endothelial-to-mesenchymal transition (EndMT) in which endothelial cells lose their characteristics and acquire mesenchymal property has recently been recognized as a driver of disease progression in wide range of pathologies. However, the regulatory mechanism of EndMT has not been fully understood. Here, we found that combined knockdown of two ETS family transcription factors, ERG and FLI1, induced EndMT. Hence, we analyzed functions of ERG and FLI1 using gene expression microarray and ChIP-seq to elucidate the regulatory mechanism of EndMT.

Publication Title

Downregulation of ERG and FLI1 expression in endothelial cells triggers endothelial-to-mesenchymal transition.

Sample Metadata Fields

No sample metadata fields

View Samples
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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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