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accession-icon GSE38309
Expression data from A549 cells after treatment with flagellin and transforming growth factor beta 1
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We have examined the changes in gene expression aftert reatment of A549 cells, a cultured alveolar epithelial cells, with flagellin and transforming growth factor beta 1.

Publication Title

Induction of epithelial-mesenchymal transition by flagellin in cultured lung epithelial cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE29367
Expression data from human squamous cell lung cancer line HARA and highly bone metastatic subline HARA-B4.
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We investigated the molecular mechanisms for osteolytic bone metastasis by selecting human lung cancer cell line subpopulations with elevated metastatic activity and validating genes that are overexpressed in these cells. A bone-seeking squamous lung cancer cell line (HARA-B4) was established by sequentially injecting parental HARA cells into the left ventricle of male 5-week-old nude mice 4 times.

Publication Title

Involvement of CXCL14 in osteolytic bone metastasis from lung cancer.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE65069
5Z-7-Oxozeanol inhibits the effect of TGFB1 on human gingival fibroblasts
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Microarray analysis was used to show that in gingival fibroblasts essentially all TGFB1 responsive genes were blocked by TAK inhibition

Publication Title

5Z-7-Oxozeanol Inhibits the Effects of TGFβ1 on Human Gingival Fibroblasts.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE110335
Glycyrrhetinic acid antagonizes pressure-induced venous remodeling in mice
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Development of spider veins is caused by the remodeling of veins located in the upper dermis and promoted by risk factors such as obesity or pregnancy that chronically increase venous pressure. We have repeatedly shown that the pressure-induced increase in biomechanical wall stress is sufficient to evoke the formation of enlarged corkscrew-like superficial veins in mice. Subsequent experimental approaches revealed that interference with endothelial- and/or smooth muscle cell activation counteracts this remodeling process. Here, we investigate whether the herbal agent glycyrrhetinic acid (GA) is a suitable candidate for that purpose given its anti-proliferative as well as anti-oxidative properties.

Publication Title

Glycyrrhetinic Acid Antagonizes Pressure-Induced Venous Remodeling in Mice.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP097752
Intergenerational programming of hepatic xenobiotic response by paternal Nicotine exposure
  • organism-icon Mus musculus
  • sample-icon 240 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Although it is increasingly accepted that some paternal environmental conditions can influence phenotypes in future generations, it generally remains unclear whether the phenotypes induced in offspring represent specific responses to particular aspects of the paternal exposure history, or whether they represent a more generic response to paternal “quality of life”. To establish a paternal effect model based on a known ligand-receptor interaction and thereby enable pharmacological interrogation of the specificity of the offspring response, we explored the effects of paternal nicotine administration on offspring phenotype in mouse. We show that chronic paternal exposure to nicotine prior to reproduction induced a broad protective response to multiple xenobiotics in the next generation. This effect manifested as increased survival following an injection of toxic levels of either nicotine or of cocaine, was specific to male offspring, and was only observed after offspring were first acclimated to sublethal doses of nicotine or cocaine. Mechanistically, the reprogrammed state was characterized by enhanced clearance of nicotine in drug-acclimated animals, accompanied by hepatic upregulation of genes involved in xenobiotic metabolism. Surprisingly, this protective effect could also be induced by paternal exposure to a nicotinic receptor antagonist as well as to nicotine, suggesting that paternal xenobiotic exposure, rather than nicotinic receptor signaling, is likely to be responsible for programming of offspring drug resistance. Taken together, our data show that paternal drug exposure can induce a protective phenotype in offspring by enhancing metabolic tolerance to xenobiotics in the environment. Overall design: Hepatocytes were isolated from 8 week-old male F1 animals from control (TA) and nicotine-exposed (NIC) fathers, and allowed to adhere to the bottom of the well for three hours. Nonadherent cells were then removed, and fresh culture medium was then added. Cells were harvested at different time points in Trizol, and total RNA was extracted. Strand specific libraries were prepared from all samples, and sequenced on Illumina NextSeq500.

Publication Title

Paternal nicotine exposure alters hepatic xenobiotic metabolism in offspring.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon GSE7509
Gene expression changes in anti-FcgRIIb treated DCs and monocytes
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The ability of dendritic cells (DCs) to activate immunity is linked to their maturation status. In prior studies we have shown that selective antibody-mediated blockade of inhibitory FcgRIIB receptor on human DCs in the presence of activating immunoglobulin (Ig) ligands leads to DC maturation and enhanced immunity to antibody-coated tumor cells. Here we show that Fcg receptor (FcgR) mediated activation of human monocytes and monocyte-derived DCs is associated with a distinct gene expression pattern, including several inflammation associated chemokines as well as type 1 interferon (IFN) response genes including the activation of signal transducer and activator of transcription 1 (STAT1).

Publication Title

Selective blockade of the inhibitory Fcgamma receptor (FcgammaRIIB) in human dendritic cells and monocytes induces a type I interferon response program.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE19400
S. aureus gene expression following AFN-1252 treatment
  • organism-icon Staphylococcus aureus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix S. aureus Genome Array (saureus)

Description

AFN-1252 is an inhibitor of fatty acid biosynthesis. Gene expression profiles were generated by microarray analysis of S. aureus cells following treatment with AFN-1252, an inhibitor of fatty acid synthesis.

Publication Title

Perturbation of Staphylococcus aureus gene expression by the enoyl-acyl carrier protein reductase inhibitor AFN-1252.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE66949
A YAP/TAZ-Regulated Molecular Signature is Associated with Oral Squamous Cell Carcinoma
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Oral squamous cell carcinoma (OSCC) is a prevalent form of cancer that develops from the epithelium of the oral cavity. OSCC is on the rise worldwide, and death rates associated with the disease are particularly high. Despite progress in understanding of the mutational and expression landscape associated with OSCC, advances in deciphering these alterations for the development of therapeutic strategies have been limited. Further insight into the molecular cues that contribute to OSCC is therefore required. Here we show that the transcriptional regulators YAP (YAP1) and TAZ (WWTR1), which are key effectors of the Hippo pathway, drive pro-tumorigenic signals in OSCC. Regions of pre-malignant oral tissues exhibit aberrant nuclear YAP accumulation, suggesting that dysregulated YAP activity contributes to the onset of OSCC. Supporting this premise, we determined that nuclear YAP and TAZ activity drives OSCC cell proliferation, survival, and migration in vitro, and is required for OSCC tumor growth and metastasis in vivo. Global gene expression profiles associated with YAP and TAZ knockdown revealed changes in the control of gene expression implicated in pro-tumorigenic signaling, including those required for cell cycle progression and survival. Notably, the transcriptional signature regulated by YAP and TAZ significantly correlates with gene expression changes occurring in human OSCCs identified by The Cancer Genome Atlas (TCGA), emphasizing a central role for YAP and TAZ in OSCC biology.

Publication Title

A YAP/TAZ-Regulated Molecular Signature Is Associated with Oral Squamous Cell Carcinoma.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE51804
Effect of W805EC nanoemulsion (NE) on global gene transcription in JawsII dendritic cells in vitro
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Nanoemulsion adjuvant affects immune gene expression in dendritic cells.

Publication Title

Distinct pathways of humoral and cellular immunity induced with the mucosal administration of a nanoemulsion adjuvant.

Sample Metadata Fields

Specimen part

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accession-icon GSE16624
Expression data from lungs of rats with pulmonary hypertension
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Pulmonary hypertension is a frequent consequence of left heart disease and congestive heart failure (CHF) and causes extensive lung vascular remodelling which leads to right ventricular failure. Functional genomics underlying this structural remodelling are unknown but present potential targets for novel therapeutic strategies. We used microarrays to detail the gene expression underlying vascular remodeling in the pathogenesis of pulmonary hypertension and identified distinct classes of up-regulated genes during this process.

Publication Title

Mast cells promote lung vascular remodelling in pulmonary hypertension.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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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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