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accession-icon GSE42007
A Kinetic Analysis of Auxin-mediated Changes in Transcript Abundance in Arabidopsis Reveals New Mediators of Root Growth and Development
  • organism-icon Arabidopsis thaliana
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Auxin-dependent transcript abundance was assayed by transferring 6 day old Arabidopsis grown on a a nylon mesh to IAA-containing or control media

Publication Title

A kinetic analysis of the auxin transcriptome reveals cell wall remodeling proteins that modulate lateral root development in Arabidopsis.

Sample Metadata Fields

Specimen part

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accession-icon GSE31561
Transcriptional analysis of organ-specific toxicity induced by a panPPAR agonist in mice: Identification of organ-specific toxicity biomarkers
  • organism-icon Mus musculus
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

In this study, we aim to identify candidate biomarkers which may be useful as surrogate indicators of toxicity for pre-clinical development of panPPAR-agonist drug candidates. Gene expression microarray, histopathology and clinical chemistry data were generated from liver, heart, kidney and skeletal muscles of three groups of mice administered with three different dosages of an experimental pan-peroxisome proliferator-activated receptor (pan-PPAR) agonist, PPM-201, for 14 days. The histopathology and clinical chemistry data were compared with the gene expression analysis and candidate biomarker genes were identified.

Publication Title

Simultaneous non-negative matrix factorization for multiple large scale gene expression datasets in toxicology.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE41833
Expression profiles of primary bone marrow derived mouse macrophages untreated and treated with LPS or LPS+PGE
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

The polarization of macrophages into an anti-inflammatory or regulatory phenotype plays an important role in resolving inflammation. PGE2 regulates macrophage polarization via a PKA dependent pathway. PKA phosphorylates SIKs, inhibiting their ability to phosphorylate CRTC3 in cells. This in turn allows CRTC3 to translocate to the nucleus where it acts as a co-activator with the transcription factor CREB to induce IL-10 transcription. In line with this we find that either genetic or pharmacological inhibition of SIKs mimics the effect of PGE2 on IL-10 production.

Publication Title

PGE(2) induces macrophage IL-10 production and a regulatory-like phenotype via a protein kinase A-SIK-CRTC3 pathway.

Sample Metadata Fields

Specimen part

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accession-icon GSE52753
Effects of fibroblast growth factors (FGF) on dissociated myelinating cultures
  • organism-icon Rattus norvegicus
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Analysis of the effects of three members of the FGF family (FGF1, FGF2 and FGF9) and bone morphogenic protein 4 (BMP4) on myelinating cultures generated from dissociated embryonic spinal cord. The results of both immediate (24 hours, T1 (24 hrs)) and long term treatments (10days, T2) give insights into the cumulative effects of sustained FGF and BMP mediated signal transduction in the pathogenesis of demyelinating diseases.

Publication Title

Fibroblast growth factor signalling in multiple sclerosis: inhibition of myelination and induction of pro-inflammatory environment by FGF9.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE44562
Fibroblast growth factor 9 inhibits remyelination via an off target effect on astrocytes in multiple sclerosis
  • organism-icon Rattus norvegicus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Failure of remyelination in multiple sclerosis (MS) is associated with inhibition of oligodendrocyte precursor (OPC) differentiation, but the cellular and molecular mechanisms involved remain poorly understood. We now report inflammatory demyelination in MS is associated with localized expression of fibroblast growth factor 9 (FGF9) by oligodendrocytes and to a lesser extent astrocytes, and demonstrate FGF9 inhibits myelination and remyelination in vitro. This inhibitory activity is reversible and due to an off target FGF9-dependent effect on astrocytes that disrupts in the growth factor milieu required to support myelination.

Publication Title

Fibroblast growth factor signalling in multiple sclerosis: inhibition of myelination and induction of pro-inflammatory environment by FGF9.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE71258
Identification of genes associated with breast cancer micrometastatic disease in bone marrow disseminated tumor cells (DTCs)
  • organism-icon Homo sapiens
  • sample-icon 126 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In this study, we assess the effect of zoledronic acid on clearance of disseminated tumour cells (DTCs) from the bone marrow in women undergoing neoadjuvant chemotherapy for breast cancer

Publication Title

CXCR4 Protein Epitope Mimetic Antagonist POL5551 Disrupts Metastasis and Enhances Chemotherapy Effect in Triple-Negative Breast Cancer.

Sample Metadata Fields

Specimen part

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accession-icon GSE36085
Regulation of Autophagy by VEGF-C axis in cancer
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

A major contributor to cancer mortality is recurrence and subsequent metastatic transformation following therapeutic intervention. In order to develop new treatment modalities or improve the efficacy of current ones it is important to understand the molecular mechanisms that promote therapy-resistance to cancer cells. One pathway that has been demonstrated to therapy resistance is autophagy, a self-digestive process that can eliminate unnecessary or damaged organelles to protect cancer cells from necrosis. Effective targeting of this pathway could lead to the development of new therapies. In our studies, we found that the VEGF-C/NRP-2 axis is involved in the activation of autophagy, which is essential for the survival of cancer cells following chemotherapy treatment. Furthermore, we identified two VEGF-C/NRP-2-regulated genes, LAMP-2 and WDFY-1 that have previously been suggested to participate in autophagy and vesicular trafficking. The upregulation of WDFY-1 upon depleted level of VEGF-C contributed to cytotoxic drug-mediated cell death. Altogether, these data suggest a link between VEGF-C/neuropilin-2 axis and cancer cell survival despite the presence of chemotherapy-induced stress.

Publication Title

Autophagy control by the VEGF-C/NRP-2 axis in cancer and its implication for treatment resistance.

Sample Metadata Fields

Cell line

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accession-icon SRP033573
HBI1 integrates hormonal and environmental signals to regulate the trade-off between growth and immunity (RNA-seq)
  • organism-icon Arabidopsis thaliana
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer

Description

The trade-off between growth and immunity is crucial for survival in plants. An antagonistic interaction has been observed between the growth-promoting hormone brassinosteroid and pathogen associated molecular pattern (PAMP) signals, which induce immunity but inhibit growth, however the underlying molecular mechanism has remained unclear. The PRE-IBH1-HBI1 triple helix-loop-helix/basic helix-loop-helix (HLH/bHLH) cascade has been shown to mediate growth responses to several hormonal and environmental signals, but its downstream targets and role in immunity remain unknown. Here, we performed genome-wide analyses of HBI1 target genes in Arabidopsis. The results show that HBI1 regulates a set of genes that largely overlaps with targets of PIFs, but displays both similar and unique transcriptional activities compared to PIFs, supporting a role in fine-tuning the network through cooperation and antagonism with other DNA-binding factors of the network. Furthermore, HBI1 also negatively regulates a subset of defense response genes. Two PAMPs, flagellin and elongation factor, repressed HBI1 expression, whereas overexpression of HBI1 reduced the PAMP-induced growth inhibition, defense gene expression, reactive oxygen species (ROS) production, and flg22-induced resistance to Pseudomonas syringae pathovar tomato DC3000. These data indicate that HBI1 is a node for crosstalk between hormone and immune pathways. This study demonstrates that the PRE-IBH1-HBI1 module integrates hormone and pathogen signals, and thus plays a central role in the balance between growth and immunity in plants. Overall design: Compare the transcriptome of HBI1-Ox and wild type.

Publication Title

The bHLH transcription factor HBI1 mediates the trade-off between growth and pathogen-associated molecular pattern-triggered immunity in Arabidopsis.

Sample Metadata Fields

Subject

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accession-icon GSE17388
Gene expression analysis of rat livers treated with pharmaceutical development compounds
  • organism-icon Rattus norvegicus
  • sample-icon 44 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome U34 Array (rgu34a)

Description

We used microarrays to analyze gene expression changes in liver after treatment of rats with two compounds from drug development (R1, R2) to identify potential effects related to hepatotoxicity.

Publication Title

Gene expression-based in vivo and in vitro prediction of liver toxicity allows compound selection at an early stage of drug development.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE10591
Expression in HepG2 cells with overexpression of TMPRSS6 or its mutant version.
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

TMPRSS6 is a type II transmembrane serine protease and is revealed by our work to be part of a low-iron sensing pathway. When animal gets iron deficient, TMPRSS6 is required to shut off hepcidin gene, so as to allow iron to be uptaken from GI tract. The mutant mouse, which was generated by ENU mutagenesis, has developed microcytic anemia. The phenotype is caused by a splicing error in Tmprss6 gene. However, the mechanism of TMPRSS6 effect remains elusive. To gain further insight into the molecular components of the TMPRSS6 signaling pathway, we overexpressed either TMPRSS6 or its mutant version of protein in human liver carcinoma cell line HepG2 cells, and compared the transcription status betweem these two treatments.

Publication Title

The serine protease TMPRSS6 is required to sense iron deficiency.

Sample Metadata Fields

No sample metadata fields

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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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