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accession-icon SRP072687
HEK293 Heat-shock experiment
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

HEK293 cells were heatshocked and differentially expressed transcripts were identified Overall design: Transcriptomes of heatshocked HEK293 cells were compared to control cells. Heatshock and control samples were treated and sequenced in triplicate.

Publication Title

RNA Directed Modulation of Phenotypic Plasticity in Human Cells.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE1727
Isolation and angiogenesis by endothelial progenitors in the fetal liver
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

While others have reported that fetal liver contains a population of endothelial progenitors based on expression of cell surface markers or culture assays, this is the first proof of a CD31+Sca1+ progenitor by demonstrating highly efficient in vivo angiogenesis and a direct connection to the host vasculature. We have developed a novel isolation method based on collagenase digestion and culture on a fetal liver-derived feeder layer and demonstrate that the feeder cells or their supernatants are required for endothelial progenitor survival and proliferation. Proteogenomic profiling of the endothelial progenitors and the feeder cells was done with tandem mass spectrometry proteomics using MudPIT and gene transcript expression profiling using high density DNA microarrays. This approach identified a number of gene transcripts, proteins and candidate growth factor pathways that are likely to be involved in endothelial progenitor growth, differentiation and angiogenesis.

Publication Title

Isolation and angiogenesis by endothelial progenitors in the fetal liver.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP167706
Genome-wide analysis of astrocyte XBP1 activation and regulation of transcriptional programs in CNS cells during EAE.
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We report XBP1 activation and regulation of pro-inflammatory signaling in astrocytes, microglia, and CNS-recruited pro-inflammatory monocytes during EAE. Overall design: Analysis of RNA expression in astrocytes, microglia, and monocytes sorted by flow cytometry. Mice transduced with astrocyte-targeting lentiviruses encoding non-targeting or Xbp1-targeting shRNAs.

Publication Title

Environmental Control of Astrocyte Pathogenic Activities in CNS Inflammation.

Sample Metadata Fields

Sex, Disease, Cell line, Subject

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accession-icon GSE102235
Regulation of gene expression by HIF-2alpha in multiple myeloma
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Proliferation of neoplastic plasma cells within the bone marrow leads to reduced oxygen availability. In response to hypoxia, the transcription factor hypoxia-inducible factor-2alpha (HIF-2) is activated and stabilised. We hypothesise that activation of HIF-2 is a central driver of multiple myeloma disease progression, leading to the induction of transcription of genes associated with angiogenesis, osteoclast activation and cell migration. In this study we assessed the affects of HIF-2 overexpression on gene expression in the human myeloma cell line LP-1.

Publication Title

HIF-2α Promotes Dissemination of Plasma Cells in Multiple Myeloma by Regulating CXCL12/CXCR4 and CCR1.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12187
Biomarkers for Early and Late Stage Chronic Allograft Nephropathy by Genomic Profiling of Peripheral Blood
  • organism-icon Homo sapiens
  • sample-icon 75 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Despite significant improvements in life expectancy of kidney transplant patients due to advances in surgery and immunosuppression, Chronic Allograft Nephropathy (CAN) remains a daunting problem. A complex network of cellular mechanisms in both graft and peripheral immune compartments complicates the non-invasive diagnosis of CAN, which still requires biopsy histology. This is compounded by non-immunological factors contributing to graft injury. There is a pressing need to identify and validate minimally invasive biomarkers for CAN to serve as early predictors of graft loss and as metrics for managing long-term immunosuppression.

Publication Title

Biomarkers for early and late stage chronic allograft nephropathy by proteogenomic profiling of peripheral blood.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE21463
NRG1/ERBB3 signaling in melanocyte Melan-Ink4a cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Neuregulin (NRG) signaling through the receptor tyrosine kinase, ERBB3, is required for embryonic development, and dysregulated signaling has been associated with cancer progression. Here, we show that NRG1/ERBB3 signaling inhibits melanocyte (MC) maturation and promotes undifferentiated, migratory and proliferative cellular characteristics. Embryonic analyses demonstrated that initial MC specification and distribution were not dependent on ERBB3 signaling. However NRG1/ERBB3 signaling was both necessary and sufficient to inhibit differentiation of later stages of MC development in culture. Analysis of tissue arrays of human melanoma samples suggests that ERBB3 signaling may also contribute to metastatic progression of melanoma as ERBB3 was phosphorylated in primary tumors compared with nevi or metastatic lesions. Neuregulin 1-treated MCs demonstrated increased proliferation and invasion and altered morphology concomitant with decreased levels of differentiation genes, increased levels of proliferation genes and altered levels of melanoma progression and metastases genes. ERBB3 activation in primary melanomas suggests that NRG1/ERBB3 signaling may contribute to the progression of melanoma from benign nevi to malignancies. We propose that targeting ERBB3 activation and downstream genes identified in this study may provide novel therapeutic interventions for malignant melanoma.

Publication Title

NRG1 / ERBB3 signaling in melanocyte development and melanoma: inhibition of differentiation and promotion of proliferation.

Sample Metadata Fields

Specimen part

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accession-icon SRP067529
Effect of mitochondria deficiency on senescence-associated gene expression
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconNextSeq500

Description

We used parkin –overexpressing MRC5 fibroblasts to investigate the role of mitochondria deficiency on senescence-associated gene expression. Overall design: RNA-seq analysis on proliferating and senescent Parkin-expressing MRC5 fibroblasts treated with CCCP (treated) or DMSO (Untreated).

Publication Title

Mitochondria are required for pro-ageing features of the senescent phenotype.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE44091
Genome-wide expression of the epithelial layer cells of mice injected with Clostridium difficile Toxin A and B
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Toxin A (TcdA) and Toxin B (TcdB), of the pathogen Clostridium difficile, are virulence factors that cause gross pathologic changes (e.g. inflammation, secretion, and diarrhea) in the infected host, yet the molecular and cellular pathways leading to observed host responses are poorly understood. To address this gap, TcdA and/or TcdB were injected into the ceca of mice and the genome-wide transcriptional response of epithelial layer cells was examined. Bioinformatic analysis of gene expression identified sets of cooperatively expressed genes. Further analysis of inflammation associated genes revealed dynamic chemokine responses.

Publication Title

In vivo physiological and transcriptional profiling reveals host responses to Clostridium difficile toxin A and toxin B.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE58225
A rat toxicogenomics study with Calcium Sensitizer EMD 82571 reveals a pleiotropic cause and adverse outcome pathway of teratogenicity
  • organism-icon Rattus norvegicus
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

The aim of reprotoxicity testing is to reveal adverse effects of chemicals and drugs on reproduction and on pre and postnatal fetal development. There is very limited data available on gene expression profiling for elucidation of the teratogenic effects of nongenotoxic teratogens. Therefore, research was undertaken to obtain knowledge on the molecular effects of MSC1096199 (previously known as EMD 82571), a calcium sensitizer that was abandoned in the preclinical development phase due to its teratogenic effects in some foetuses. Pregnant wistar rats were dose daily with either MSC1096199 (50 or 150 mg/kg) or Retinoic acid (12 mg/kg) on gestational days 6-17. Microarray experiment were performed using four different tissues (maternal liver, embryo liver (GD20), embryo bone (GD20), and whole embryo (GD12)) under four different conditions (vehicle, low dose and high dose of MSC1096199 and Retinoic acid) to determine the drug regulated genes. In the high dose treatment group, approximately 58% of the fetuses showed malformations i.e. exencephaly and agnathia, and toxicogenomics evidenced that the genes critically involved in osteogenesis, odontogenesis and extra cellular matrix components to be significantly regulated by MSC1096199, therefore providing a molecular rational for the observed teratogenic effects.

Publication Title

A rat toxicogenomics study with the calcium sensitizer EMD82571 reveals a pleiotropic cause of teratogenicity.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE22523
Analysis of vitamin D response element binding protein target genes reveals a role for vitamin D in osteoblast mTOR signaling
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Heterogeneous nuclear ribonucleoprotein (hnRNP) C1/C2 plays a pivotal role in vitamin D receptor (VDR) signaling by acting as a vitamin D response element (VDRE)-binding protein (VDRE-BP). Transcriptional regulation by active 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) involves occupancy of VDRE by VDRE-BP or 1,25(OH)2D3 bound-VDR. This relationship is disrupted by over-expression of VDRE-BP and can cause a form of human hereditary vitamin D-resistant rickets (HVDRR). DNA array analyses using B-cells from an HVDRR patient and matched control defined a sub-cluster of genes where 1,25(OH)2D3-regulated transcription was abrogated by over-expression of VDRE-BP. Amongst these, the DNA-damage-inducible transcript 4 (DDIT4), an inhibitor of mammalian target of rapamycin (mTOR) signaling, was also induced by 1,25(OH)2D3 in human osteoblasts.

Publication Title

Gene targeting by the vitamin D response element binding protein reveals a role for vitamin D in osteoblast mTOR signaling.

Sample Metadata Fields

Sex, Specimen part, Subject

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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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