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accession-icon SRP128913
Next Generation Sequencing Facilitates Quantitative Analysis of the Effect of GM-CSF on the Transcriptomes of Alveolar and Exudative Lung Macrophages from Influenza-infected C57BL/6 Mice
  • organism-icon Mus musculus
  • sample-icon 26 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The transcriptomes of FACS-sorted siglec-F+ alveolar macrophages and siglec-f- CD11b+ exudative macrophages from inducible airway GM-CSF over-expressing transgenic mice (DTGM) were compared to non-inducible littermate controls during influenza A virus infection. Overall design: Examination of effect of GM-CSF on airway macrophages during influenza A virus infection

Publication Title

GM-CSF overexpression after influenza a virus infection prevents mortality and moderates M1-like airway monocyte/macrophage polarization.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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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

View Samples
accession-icon SRP065219
Transcriptome response to 4h IL-1b stimulation of primary chondrocytes
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Using RNA sequencing (Illumina Hi-Seq 2000 sequencer) we report the transcriptome profile of primary human chondrocytes isolated from patients with hip osteoarthritis (OA), and the transcriptome response of these cells to 4h stimulation with IL-1ß (1ng/ml). In total, 983 long non-coding RNAs (lncRNAs) were identified, which included 642 intergenic lncRNAs (lincRNAs), 124 antisense and pseudogenes. Less than 4% of the identified lncRNAs overlapped with putative eRNAs regions, and visual inspection showed that they were uni-directional and multi-exonic. Upon IL-1ß stimulation 499 protein-coding genes were differentially expressed, and 158 lncRNAs were differentially expressed, including 92 lincRNAs, 13 antisense and 18 psudogenes. This study demonstrates that IL-1ß induces a rapid and widespread change in the transcriptome of the primary human OA chondrocyte. Overall design: RNA sequencing analysis of primary human chondrocytes isolated from n=3 patients with hip osteoarthritis, with and without 4h IL-1b (1ng/ml) stimulation

Publication Title

Long Intergenic Noncoding RNAs Mediate the Human Chondrocyte Inflammatory Response and Are Differentially Expressed in Osteoarthritis Cartilage.

Sample Metadata Fields

No sample metadata fields

View Samples
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 GSE56504
Loss of nuclear TDP-43 in ALS causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurons
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Loss of nuclear TDP-43 in amyotrophic lateral sclerosis (ALS) causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurones.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE33855
Loss of nuclear TDP-43 in ALS causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurons [fibroblasts]
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

Aims: Loss of nuclear TDP-43 characterises sporadic and most familial forms of amyotrophic lateral sclerosis (ALS). TDP-43 (encoded by TARDBP) has multiple roles in RNA processing. We aimed to determine whether 1) RNA splicing dysregulation is present in lower motor neurons in ALS and in a motor neuron-like cell model, and 2) TARDBP mutations (mtTARDBP) are associated with aberrant RNA splicing using patient-derived fibroblasts.

Publication Title

Loss of nuclear TDP-43 in amyotrophic lateral sclerosis (ALS) causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurones.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE56500
Loss of nuclear TDP-43 in ALS causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurons [LCM]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

Aims: Loss of nuclear TDP-43 characterises sporadic and most familial forms of amyotrophic lateral sclerosis (ALS). TDP-43 (encoded by TARDBP) has multiple roles in RNA processing. We aimed to determine whether 1) RNA splicing dysregulation is present in lower motor neurons in ALS and in a motor neuron-like cell model, and 2) TARDBP mutations (mtTARDBP) are associated with aberrant RNA splicing using patient-derived fibroblasts.

Publication Title

Loss of nuclear TDP-43 in amyotrophic lateral sclerosis (ALS) causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurones.

Sample Metadata Fields

Specimen part

View Samples
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

View Samples
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

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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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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