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accession-icon GSE4607
Systemic inflammatory response syndrome and septic shock
  • organism-icon Homo sapiens
  • sample-icon 55 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Goal of the experiment: To identify correlated genes, pathways and groups of patients with systemic inflammatory response syndrome and septic shock that is indicative of biologically important processes active in these patients.

Publication Title

Genome-level expression profiles in pediatric septic shock indicate a role for altered zinc homeostasis in poor outcome.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP019222
Epstein-Barr virus maintains lymphomas via its miRNAs
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Epstein-Barr virus (EBV) has evolved exquisite controls over its host cells, human B lymphocytes, not only directing these cells during latency to proliferate and thereby expand the pool of infected cells, but also to survive and thereby persist for the lifetime of the infected individual. Although these activities ensure the virus is successful, they also make the virus oncogenic, particularly when infected people are immunosuppressed. Here we show, strikingly, that one set of EBV’s miRNAs both sustain BL (Burkitt’s lymphoma) cells in the absence of other viral oncogenes and promote the transformation of primary B lymphocytes. Burkitt’s Lymphoma cells were engineered to lose EBV and found to die by apoptosis and could be rescued by constitutively expressing viral miRNAs in them. Two of these EBV miRNAs were found to target Caspase 3 to inhibit apoptosis at physiological concentrations. Overall design: Examination of RISC associated transcripts under 4 conditions in Sav S1-1 cells

Publication Title

Epstein-Barr virus maintains lymphomas via its miRNAs.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon GSE13110
MYB silencing in CD34+ progenitor cells
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

The c-Myb transcription factor is highly expressed in immature hematopoietic cells and down-regulated during differentiation. To define the role of c-Myb in human hematopoietic lineage commitment, we studied the effects of its silencing during the commitment of human CD34+ Hematopoietic stem/progenitor cells. In CD34+ cells c-Myb silencing determined a cell cycle arrest in G0/G1 phase which strongly decreased the clonogenic efficiency, togheter with a reduction of erythroid colonies coupled with an increase of the macrophage and megakaryocyte ones. Moreover, morphological and flow cytometry data supported the preferential macrophage and megakaryocyte differentiation of c-Myb-silenced CD34+ cells. Taken together our data indicate that c-Myb is essential for the commitment along the erythroid and granulocyte lineages but not for the macrophage and megakaryocyte differentiation. Gene expression profiling of c-Myb-silenced CD34+ cells identified some potential c-Myb targets which can account for these effects, to study by Chromatin Immunoprecipitation and Luciferase Reporter Assay.

Publication Title

c-myb supports erythropoiesis through the transactivation of KLF1 and LMO2 expression.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE21943
MYB silencing in CD14-myeloblasts
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

The c-Myb transcription factor is highly expressed in immature hematopoietic cells and down-regulated during differentiation. To define the role of c-Myb during the terminal differentiation of hematopoietic precursors, we studied the effects of its silencing in human primary CD14-myeloblasts, which maintain a granulo-monocyte differentiation bipotentiality. c-Myb-silenced myeloblasts were blocked in the G1 phase of the cell cycle at 24 hours post-nucleofection and subsequently were forced towards macrophage differentiation, as demonstrated by immunophenotypic and morphological analysis. Indeed, c-Myb-silenced CD14- cells differentiate to macrophage even after the treatment with ATRA 10-6 M, demonstrating that the c-Myb knockdown strongly impairs the ability of myeloblasts to differentiate to granulocytes. Gene expression profiling of c-Myb-silenced CD14- cells identified some potential c-Myb targets that can account for these effects.

Publication Title

c-myb supports erythropoiesis through the transactivation of KLF1 and LMO2 expression.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE10467
Investigating genes regulated by mir-155 in a mouse macrophage cell line
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Mammalian microRNAs (miRNAs) are emerging as key regulators of the development and function of the immune system. Here, we report a strong but transient induction of miR-155 in mouse bone marrow after injection of bacterial lipopolysaccharide (LPS) correlated with granulocyte/monocyte (GM) expansion. Demonstrating the sufficiency of miR-155 to drive GM expansion, enforced expression in mouse bone marrow cells caused GM proliferation in a manner reminiscent of LPS treatment. However, the mir-155-induced GM populations displayed pathological features characteristic of myeloid neoplasia. Extending possible relevance to human disease, miR-155 was overexpressed in the bone marrow of patients with acute myeloid leukemia (AML). Furthermore, miR-155 repressed a subset of genes implicated in hematopoietic development and disease. These data implicate miR-155 as a contributor to physiological GM expansion during inflammation and to certain pathological features associated with AML, emphasizing the importance of proper miR-155 regulation in developing myeloid cells during times of inflammatory stress.

Publication Title

Sustained expression of microRNA-155 in hematopoietic stem cells causes a myeloproliferative disorder.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE31040
Gene expression analysis of human lymphoblastoid cell lines
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Human lymphoblastoid cell lines (EBV-immortalised B cells, LcL) obtained from subjects of different age (young 28-40 years, centenarians >95 years) were analysed for gene expression at basal culture conditions and after 48 hours of serum starvation. Lymphoid B cells from centenarians were more resistant to apoptosis induction and displayed a more developed lysosomal compartment, the most critical component of phagic machinery. In addition, cells from centenarians were capable of engulfing and digesting other cells, i.e. their siblings (even entire cells). This behavior was improved by nutrient deprivation, but strikingly, it was unaffected by the autophagy-modulating drugs rapamycin, an autophagy inducer, and 3-methyladenine, an autophagy inhibitor.

Publication Title

Survival features of EBV-stabilized cells from centenarians: morpho-functional and transcriptomic analyses.

Sample Metadata Fields

Sex, Age, Specimen part, Subject

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accession-icon GSE89156
Gene expression profile (GEP) of miR-34a-5p-overexpressing CD34+ HPCs
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Primary Myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by hyperplastic megakaryopoiesis and myelofibrosis. Through a gene expression profile (GEP) study we recently highlighted the upregulationof miR-34a-5p in PMF versus healthy donor (HD) CD34+ hematopoietic progenitor cells (HPCs). To shed some light into the role of miR-34a-5p in PMF pathogenesis, here we unravelled the effects of the overexpression of miR-34a-5p in HPCs forcing its expression in HPCs.

Publication Title

Role of miR-34a-5p in Hematopoietic Progenitor Cells Proliferation and Fate Decision: Novel Insights into the Pathogenesis of Primary Myelofibrosis.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon SRP132709
Whole blood transcriptome analysis of Septic shock patients according to early therapy response
  • organism-icon Homo sapiens
  • sample-icon 64 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx, Illumina HiSeq 2500

Description

Septic shock is the most severe complication of sepsis, associated with high mortality. The patient's response to supportive therapy is very heterogeneous and the underlying mechanisms are still elusive. In order to identify which are the actors (genes and pathways) that play a role in establishing the response, we investigate the whole blood transcriptome in septic shock patients with positive and negative responses to early supportive hemodynamic therapy, assessed by changes in SOFA scores within the first 48 hours from ICU admission. We pinpointed genes and pathways that are differently modulated and enriched respectively within 48hrs between responders and non-responders. Overall design: We analyzed 31 patients (17 Responders and 14 Not Responders to early therapy). For each patient, 2 samples were collected. In particular the first sample (T1) collected within 16 hours from ICU admission whereas the second (T2) collected within 48 hours from ICU admission. Experimental groups (Responders and Not Responders) are defined accordingly with SOFA scores improvements within 48 hours.

Publication Title

Identification of a transcriptome profile associated with improvement of organ function in septic shock patients after early supportive therapy.

Sample Metadata Fields

Specimen part, Subject, Time

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accession-icon GSE18552
CDK inhibitors and flavopiridol profiling on A2780 and MCF7 cells
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Discovery of drug mode of action and drug repositioning from transcriptional responses.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE19638
Compounds profiling on MCF7
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The effects of several compounds on the MCF7 human adenocarcinoma mammary cell line were analysed by gene expression profiling.

Publication Title

Discovery of drug mode of action and drug repositioning from transcriptional responses.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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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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