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accession-icon GSE35240
Gene expression in mitotic tissues of Drosophila larvae without centrosomes or too many centrosomes
  • organism-icon Drosophila melanogaster
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Centrosome defects are a common feature of many cancers. Surprisingly, flies can proceed through the majority of development without centrosomes or with amplified centrosomes in most of their cells. It is unclear whether this is because centrosome defects do not cause many problems in Drosophila cells, or because they can adapt to cope with any problems that arise. Indeed, centrosome loss and centrosome amplification predispose fly brain cells to form tumours. Here we assess how centrosome loss or centrosome amplification perturbs cell physiology by profiling the global transcriptome of Drosophila larval brains and imaginal discs that either lack centrosomes or have too many centrosomes.

Publication Title

Centrosome loss or amplification does not dramatically perturb global gene expression in Drosophila.

Sample Metadata Fields

Specimen part

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accession-icon GSE21511
EWS-FLI1 reactivates a neural crest stem cell program in human neural crest-derived mesenchymal stem cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Ewing sarcoma family of tumors (ESFT) are aggressive bone and soft tissue tumors of unknown cellular origin. Most ESFT express EWS-FLI1, a chimeric protein which functions as a growth-promoting oncogene in ESFT but is toxic to most normal cells. A major difficulty in understanding EWS-FLI1 function has been the lack of an adequate model in which to study EWS-FLI1-induced transformation. Although the cell of origin of ESFT remains elusive, both mesenchymal (MSC) and neural crest (NCSC) have been implicated. We recently developed the tools to generate NCSC from human embryonic stem cells (hNCSC). In the current study we used this model to test the hypothesis that neural crest-derived stem cells are the cells of origin of ESFT and to evaluate the consequences of EWS-FLI1 expression on human neural crest biology.

Publication Title

Modeling initiation of Ewing sarcoma in human neural crest cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE9728
COP9 signalosome (csn) mutant analysis
  • organism-icon Arabidopsis thaliana
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Transcript profiling analysis of csn3-1, csn4-1 and csn5 (csn5a-2 csn5b) light grown and dark grown mutant seedlings compared to light grown and dark grown wild type using Arabidopsis ATH1 GeneChip array

Publication Title

The Arabidopsis COP9 signalosome is essential for G2 phase progression and genomic stability.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE26669
Expression data of alloantigen stimulated splenocytes treated with leukocyte costimulatory blockade antibodies or no treatment
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To elucidate the gene expression footprint of antigenically challenged T-cells which had been treated with anti-LFA-1, CTLA4Ig, anti-CD40-ligand antibodies, we performed microarray gene expression analysis comparing the expression profile of costimulatory blockade treated and untreated responder T-cells.

Publication Title

Short-term immunosuppression promotes engraftment of embryonic and induced pluripotent stem cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE103382
Expresson of CD271 HIGH and LOW populations in melanoma cells during invasion
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

Human engeneered skin carrying GFP positive melanoma cells was transplanted in immunocompromised rats.

Publication Title

low neurotrophin receptor CD271 regulates phenotype switching in melanoma.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE76598
Profiling of nave and memory Tregs
  • organism-icon Homo sapiens
  • sample-icon 51 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Changes in Treg function are difficult to quantify due to the lack of Treg-exclusive markers in humans and the complexity of functional experiments. We sorted naive and memory human Tregs and conventional T cells, and identified genes that identify human Tregs regardless of their state of activation. We developed this Treg signature using Affymetrix human genome U133A 2.0 microarrays.

Publication Title

A Regulatory T-Cell Gene Signature Is a Specific and Sensitive Biomarker to Identify Children With New-Onset Type 1 Diabetes.

Sample Metadata Fields

Treatment, Subject

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accession-icon GSE6119
Exogenous Glucosamine Globally Protects Chondrocytes from the Arthritogenic Effects of IL-1beta
  • organism-icon Rattus norvegicus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Glucosamine proved to be a potent, broad-spectrum inhibitor of IL-1beta. Of the 2,813 genes whose transcription was altered by IL-1beta stimulation (p<0.0001), glucosamine significantly blocked the response in 2,055 (~73%). Glucosamine fully protected the chondrocytes from IL-1-induced expression of inflammatory cytokines, chemokines and growth factors as well as proteins involved in PGE2 and NO synthesis. It also blocked the IL-1-induced expression of matrix specific proteases such as MMPs -3,-9,-10,-12 and ADAMTS-1.

Publication Title

Exogenous glucosamine globally protects chondrocytes from the arthritogenic effects of IL-1beta.

Sample Metadata Fields

Age

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accession-icon SRP071611
Analysis of the expression profile of skin macrophages FACS-sorted from mice overexpressing activin and/or oncogenes of human papilloma virus 8 in keratinocytes.
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We have shown that activin promoted skin tumorigenesis in mice induced by the human papilloma virus 8 oncogenes. Activin attracted blood monocytes to the skin as revealed by depletion of CCR2-positive monocytes. To determine if activin also altered the gene expression profile of these cells, we performed RNA-Sequencing of macrophages FACS-sorted from the pre-cancerous ear skin. We have found that activin induces a pro-migratiory, pro-angiogenic and pro-tumorigenic genes in skin macrophages in vivo. This largely contributes to the pro-tumorigenic function of activin, since macrophage depletion delayed spontaneous tumorigenesis in HPV8-transgenic mice by reducing keratinocyte proliferation and angiogenesis. Overall design: F4/80+CD11b+CD45+ cells were FACS-sorted from the pre-cancerous ear skin of wt/wt, HPV8/wt, wt/Act and HPV8/Act mice and their expression profile was analysed by RNA-Sequencing. Experiment was performed in triplicates, for each replicate ear skin of 3-6 mice of corresponding genotype was pooled.

Publication Title

Activin promotes skin carcinogenesis by attraction and reprogramming of macrophages.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP154834
RNA-seq profile of expanded human ST2-transduced Tregs cultured with IL-2 and TCR in the presence or absence of IL-33
  • organism-icon Homo sapiens
  • sample-icon 32 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Because of the extensive data in mice supporting the concept that ST2+ Tregs might have desirable therapeutic properties, including tissue repair function, high suppressive capacity, and enhanced stability, we engineered human blood Tregs to constitutively express ST2 (IL-33R). Here we used RNA sequencing to explore the effects of short-term culture with IL-33 on human ST2-transduced Tregs. Overall design: Human naive Tregs flow-sorted from 4 independent donors were lentivirally transduced with ST2, expanded for 13 days, then stimulated with IL-2 and TCR (16 h) or IL-2, TCR, and IL-33 (16 h).

Publication Title

Innate Control of Tissue-Reparative Human Regulatory T Cells.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon GSE45593
GENOMICS TO IDENTIFY HLA IDENTICAL RENAL TRANSPLANT TOLERANCE SIGNATURES
  • organism-icon Homo sapiens
  • sample-icon 46 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Immunosuppression is needed in HLA identical sibling renal transplantation. We conducted a tolerance trial in this patient cohort using Alemtuzumab induction, donor hematopoietic stem cells, tacrolimus/mycophenolate immunosuppression converted to sirolimus, planning complete drug withdrawal by 24 months post-transplantation. After an additional 12 months with no immunosuppression, normal biopsies and renal function, recipients were considered tolerant. Twenty recipients were enrolled. Of the first 10 (>36 months post-transplantation), 5 had immunosuppression successfully withdrawn for 16-36 months (tolerant), 2 had disease recurrence and 3 had subclinical rejection in protocol biopsies (non-tolerant). Microchimerism disappeared after 1 year, and CD4+CD25highCD127-FOXP3+ T cells and CD19+IgD/M+CD27- B cells increased to 5 years post-transplantation in both groups, whereas immune/inflammatory gene expression pathways in the peripheral blood and urine were differentially downregulated in tolerant compared to non-tolerant recipients. Therefore, in this HLA identical renal transplant tolerance trial, absent chimerism, Treg and Breg immunophenotypes were indistinguishable between tolerant and non-tolerant recipients, but global genomic changes indicating immunomodulation were observed only in tolerant recipients.

Publication Title

Genomic biomarkers correlate with HLA-identical renal transplant tolerance.

Sample Metadata Fields

Specimen part, Time

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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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