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accession-icon E-MEXP-239
Transcription profiling of mouse wild type immortalized fibroblasts
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2), Affymetrix Murine Genome U74B Version 2 Array (mgu74bv2)

Description

Cultured wild-type immortalized fibroblasts transcriptome

Publication Title

JunD reduces tumor angiogenesis by protecting cells from oxidative stress.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE26869
Regulation of myogenic progenitor proliferation in human fetal skeletal muscle by BMP4 and its antagonist Gremlin.
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Analysis of the transcriptome of mononuclear side population (SP) and main population (MP) cells of human fetal skeletal muscle from 12 human subjects of gestational age 14-18 weeks.

Publication Title

Regulation of myogenic progenitor proliferation in human fetal skeletal muscle by BMP4 and its antagonist Gremlin.

Sample Metadata Fields

Specimen part

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accession-icon GSE38290
Functional analysis of ABCB5 in melanoma cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Functional analysis of ABCB5 in A375 and G3361 melanoma cells, by comparing stably-transfected controls to ABCB5-shRNA-targeted cells.

Publication Title

ABCB5 maintains melanoma-initiating cells through a proinflammatory cytokine signaling circuit.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE29664
DNA microarray analysis and functional profile of pituitary transcriptome under core-clock protein BMAL1 control
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

To find BMAL1-regulated genes in mice pituitary gland we performed a differential microarray from wild-type vs Bmal1-/- knock-out mice

Publication Title

Chromatin remodeling as a mechanism for circadian prolactin transcription: rhythmic NONO and SFPQ recruitment to HLTF.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP136108
RNA-seq of nine primary human cell types exposed in vitro to methylprednisolone
  • organism-icon Homo sapiens
  • sample-icon 130 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Illumina HiSeq 3000

Description

Glucocorticoids remain the most widely used class of anti-inflammatory and immunosuppressive agents. They act primarily by binding to the glucocorticoid receptor, resulting in direct and indirect effects on gene expression. The current understanding of glucocorticoid effects on transcription in human cells is based mostly on studies of cancer cell lines, immortalized cell lines, or highly mixed populations of primary cells (such as peripheral blood mononuclear cells). To advance the understanding of the transcriptome-wide effects of glucocorticoids on highly pure populations of primary human cells, we performed RNA-seq on nine such cell populations at two time points after in vitro exposure to methylprednisolone or vehicle. Overall design: Nine cell types were studied: four hematopoietic (circulating B cells, CD4+ T cells, monocytes, and neutrophils) and five non-hematopoietic (endothelial cells, fibroblasts, myoblasts, osteoblasts, and preadipocytes). Each cell type was obtained from a separate cohort of 4 unrelated healthy human donors (4 biological replicates per cell type: BR1 - BR4). Cells form each donor were independently cultured and exposed in vitro to glucocorticoid or vehicle. Non-hematopoietic cells were incubated until the early plateau phase of growth, then exposed to methylprednisolone or vehicle. Hematopoietic cells were collected from peripheral blood, purified by magnetic selection (negative selection for B cells, CD4+ T cells and neutrophils; positive selection for monocytes). Purified B cells, CD4+ T cells, and monocytes were incubated overnight, then exposed to methylprednisolone or vehicle. Purified neutrophils were cultured for 4 hours, then exposed to methylprednisolone or vehicle. Ethanol was used as a vehicle for methylprednisolone. Estimated final concentrations were 8500 mcg/L (22.7 mcM) for methylprednisolone and 0.07% (15.57 mM) for ethanol (vehicle). For each cell type, samples were collected at two time points after treatment with methylprednisolone or vehicle: 2 hours and 6 hours. Samples were collected into TRIzol reagent and frozen at -80°C prior to RNA extraction. RNA-seq data for all samples is made available in this GEO Series.

Publication Title

Immune regulation by glucocorticoids can be linked to cell type-dependent transcriptional responses.

Sample Metadata Fields

Specimen part, Subject, Time

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accession-icon GSE26569
VEGFR-1 expressed by malignant melanoma initiating cells is required for tumor growth
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Melanoma growth is driven by malignant melanoma initiating cells (MMIC) identified by expression of the ATP-binding cassette (ABC) member, ABCB5. ABCB5+ melanoma subpopulations have been shown to overexpress the vasculogenic differentiation markers CD144 (VE-cadherin) and TIE-1 and are associated with CD31-negative vasculogenic mimicry (VM), an established biomarker associated with increased patient mortality. Here we identify a critical role for VEGFR-1 signaling in ABCB5+ MMIC-dependent VM and tumor growth. Global gene expression analyses, validated by mRNA and protein determinations, revealed preferential expression of VEGFR-1 on ABCB5+ tumor cells purified from clinical melanomas and established melanoma lines. In vitro, VEGF induced in a VEGFR-1-dependent manner expression of CD144 in ABCB5+ subpopulations that constitutively expressed VEGFR-1, but not in ABCB5- bulk populations that were predominantly VEGFR-1-negative. In vivo, melanomaspecific shRNA-mediated knockdown of VEGFR-1 blocked the development of ABCB5+ VM morphology and inhibited ABCB5+ VM-associated production of the secreted melanoma mitogen, laminin. Moreover, melanoma-specific VEGFR-1 knockdown markedly inhibited tumor growth (by >90%). Our results demonstrate that VEGFR-1 function in MMIC regulates VM and associated laminin production, and show that this function represents one mechanism through which MMIC promote tumor growth.

Publication Title

VEGFR-1 expressed by malignant melanoma-initiating cells is required for tumor growth.

Sample Metadata Fields

Specimen part

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accession-icon SRP073501
Complement protein C1q modulates macrophage molecular signaling and inflammatory responses during ingestion of atherogenic lipoproteins
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

C1q suppresses JAK-STAT signal transduction and activates PPAR-mediated transcription in macrophages during clearance of modified forms of LDL leading to a reduction in inflammatory response. Overall design: Human monocyte-derived macrophages (HMDM) were incubated with either oxidized (oxLDL) or acetylated low-density lipoprotein (acLDL) in the presence or absence of C1q for 3 hours. Total RNA was extracted using the Qiagen RNeasy Mini Kit. RNA libraries were constructed using the Illumina TruSeq Stranded mRNA Sample Preparation Kit. Sequences were aligned to a reference genome (hg38), RPKM and raw counts were determined using CASAVA version 1.8.2.

Publication Title

Transcriptome data and gene ontology analysis in human macrophages ingesting modified lipoproteins in the presence or absence of complement protein C1q.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP213158
Niche stiffness underlies the aging of CNS progenitor cells.
  • organism-icon Rattus norvegicus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Next generation sequencing of OPCs grown on stiff and soft hydrogels Overall design: Illumina HiSeq4000 PE150 Sequencing

Publication Title

Niche stiffness underlies the ageing of central nervous system progenitor cells.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP055101
Transcriptomic analysis of cultured corneal endothelial cells as a validation for their use in cell-replacement therapy
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

The corneal endothelium plays a primary role in maintaining corneal homeostasis and clarity, and must be surgically replaced with allogenic donor corneal endothelium in the event of visually significant dysfunction. However, a worldwide shortage of donor corneal tissue has led to a search for alternative sources of transplantable tissue. Cultured human corneal endothelial cells (HCEnC) have been shown to restore corneal clarity in experimental models of corneal endothelial dysfunction in animal models, but characterization of cultured HCEnC remains incomplete. To this end, we utilized next-generation RNA sequencing technology to compare the transcriptomic profile of ex vivo human corneal endothelium (evHCEnC) with that of primary HCEnC and HCEnC lines, and to determine the utility of cultured and immortalized corneal endothelial cells as models of in vivo corneal endothelium. Multidimensional analyses of the transcriptome datasets demonstrated that primary HCEnC have a closer relationship to evHCEnC than do immortalized HCEnC. Subsequent analyses showed that the majority of the genes specifically expressed in HCEnC (not expressed in ex vivo corneal epithelium or fibroblasts) demonstrated a marked variability of expression in cultured cells compared with evHCEnC. In addition, genes associated with either corneal endothelial cell function or corneal endothelial dystrophies were investigated. Significant differences in gene expression and protein levels were observed in the cultured cells compared with evHCEnC for each of the genes tested except for AGBL1 and LOXHD1, which were not detected by RNA-seq or qPCR. Our transcriptomic analysis suggests that at a molecular level primary HCEnC most closely resemble evHCEC and thus represent a viable therapeutic option for managing corneal endothelial dysfunction. Our findings also suggest that investigators should perform an assessment of the entire transcriptome of cultured HCEnC prior to determination of the potential clinical utility of the cultured HCEnC for the management of corneal endothelial cell failure. Overall design: Transcriptomes from ex vivo corneal endothelium, primary cultures and three cell lines were compared. Three samples of each endothelial cell group were submitted for RNA sequencing for a total of 15 samples. The transcriptome for the ex vivo corneal endothelium was used as the reference (i.e., proxy for in vivo corneal endothelium). Transcript abundances for a subset of genes associated with corneal endothelial cell function or disease were validated with qPCR and western blot. Samples of ex vivo endothelium used for validation were independent replicates not used for RNA-sequencing.

Publication Title

Transcriptomic Analysis of Cultured Corneal Endothelial Cells as a Validation for Their Use in Cell Replacement Therapy.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE8745
Low R:FR treatment at 16 and 22 degrees
  • organism-icon Arabidopsis thaliana
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

The purpose of this experiment was to identify genes responding differently to a 24 h low red to far red ratio (R:FR) treatment in plants grown at 16 and 22 degrees

Publication Title

Light-quality regulation of freezing tolerance in Arabidopsis thaliana.

Sample Metadata Fields

Age

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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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