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accession-icon GSE69555
Gene expression analyses of miR-99b and miR-330-3p overexpression in Natural killer cells
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

In order to define the targets of two miRNA overexpressed in NK cells in CFS/ME paitents, miRNA precursors for hsa-miR-99b and hsa-miR-330-3p were transfected in to buffy coat derived Natural Killer cells isolated by negative magnetic selection.

Publication Title

MicroRNAs hsa-miR-99b, hsa-miR-330, hsa-miR-126 and hsa-miR-30c: Potential Diagnostic Biomarkers in Natural Killer (NK) Cells of Patients with Chronic Fatigue Syndrome (CFS)/ Myalgic Encephalomyelitis (ME).

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE36555
Host-influenza A virus(infA) interactions
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Temporal- and strain-specific host microRNA molecular signatures associated with swine-origin H1N1 and avian-origin H7N7 influenza A virus infection.

Sample Metadata Fields

Cell line

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accession-icon GSE36553
mRNA profiling during infection with H1N1 influenza A virus (A/Mexico/InDRE4487/H1N1/2009)
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

MicroRNAs (miRNAs) repress the expression levels of genes by binding to mRNA transcripts, acting as master regulators of cellular processes. Differential expression of miRNAs has been linked to viral-associated diseases involving members of the hepacivirus, herpesvirus, and retrovirus families. In contrast, limited biological and molecular information has been reported on the potential role of cellular miRNAs in the lifecycle of influenza A viruses (infA). In this study, we hypothesize that elucidating the miRNA expression signatures induced by low-pathogenic swine-origin influenza A virus (S-OIV) pandemic H1N1 (2009) and highly pathogenic avian-origin (A-OIV) H7N7 (2003) infections could reveal temporal and strain-specific miRNA fingerprints during the viral lifecycle, shedding important insights into the potential role of cellular miRNAs in host-infA interactions. Using a microfluidic microarray platform, we profiled cellular miRNA expression in human A549 cells infected with S- and A-OIVs at multiple time-points during the viral lifecycle, including global gene expression profiling during S-OIV infection. Using target prediction and pathway enrichment analyses, we identified the key cellular pathways associated with the differentially expressed miRNAs and predicted mRNA targets during infA infection, including immune system, cell proliferation, apoptosis, cell cycle, and DNA replication and repair. By identifying the specific and dynamic molecular phenotypic changes (microRNAome) triggered by S- and A-OIV infection in human cells, we provide experimental evidence demonstrating a series of temporal- and strain-specific host molecular responses involving different combinatorial contributions of multiple cellular miRNAs. Our results also identify novel potential exosomal miRNA biomarkers associated with pandemic S-OIV and deadly A-OIV-host infection.

Publication Title

Temporal- and strain-specific host microRNA molecular signatures associated with swine-origin H1N1 and avian-origin H7N7 influenza A virus infection.

Sample Metadata Fields

Cell line

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accession-icon GSE20037
cdr2 siRNA knockdown during passage through mitosis: HeLa cells, Rat1 wild type and c-myc null cells
  • organism-icon Homo sapiens, Rattus norvegicus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

[Hela cells]: We performed cdr2 knockdown with a pool of 4 cdr2-specific siRNAs to test whether cdr2 may regulate c-myc target genes as cells passage through mitosis.

Publication Title

The onconeural antigen cdr2 is a novel APC/C target that acts in mitosis to regulate c-myc target genes in mammalian tumor cells.

Sample Metadata Fields

Cell line

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accession-icon GSE19556
Transcriptional program of terminal granulocytic differentation
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

To characterize the transcriptional program that governs terminal granulocytic differentation in vivo, we performed comprehensive microarray analysis of human bone marrow population highly enriched for promyelocytes, myelocytes / metamyelocytes and neotrophils.

Publication Title

Human neutrophils secrete bioactive paucimannosidic proteins from azurophilic granules into pathogen-infected sputum.

Sample Metadata Fields

Specimen part

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accession-icon GSE19652
Effector T cells driving monophasic vs relapse/remitting experimental autoimmune uveitis show unique pathway signatures
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Experimental autoimmune uveitis (EAU) in Lewis rats is a model for the clinical heterogeneity of human uveitis. The autoantigens inducing disease in the rat are also seen in human disease. Depending upon the specific autoantigen used, the experimental disease course can be either monophasic or relapsing/remitting and appears to be dictated by the T cell effector phenotype elicited. We investigated potential differences between monophasic and relapsing/remitting effector T cells using transcriptomic profiling and pathway analysis. RNA samples isolated from three independent T cell lines derived from each specificity where analyzed by microarrays.

Publication Title

Effector T cells driving monophasic vs. relapsing/remitting experimental autoimmune uveitis show unique pathway signatures.

Sample Metadata Fields

Specimen part

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accession-icon GSE14825
Expression data from rhabdomyosarcoma cells expressing Myod and E-protein heterodimer and controls
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Rhabdomyosarcomas (RMS) are characterized by expression of myogenic specification genes, such as MyoD and/or Myf5, as well as their bHLH partners for heterodimerization, the E-proteins. We have shown that expression of a forced heterodimer of MyoD with one of the E2A proteins, E12, leads to differentiation in a RMS cell culture model when exposed to low serum conditions.

Publication Title

MyoD and E-protein heterodimers switch rhabdomyosarcoma cells from an arrested myoblast phase to a differentiated state.

Sample Metadata Fields

Cell line

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accession-icon GSE8836
CLL in Em-TCL1 mice provides a biologically relevant model to unravel and reverse immune deficiency in human cancer.
  • organism-icon Mus musculus
  • sample-icon 56 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Immune deficiency is common in cancer, but the biological basis for this and ways to reverse it remains elusive. Here we present a mouse model of B cell chronic lymphocytic leukemia (CLL) that recapitulates changes in the non-malignant circulating T cells seen in patients with this illness.1 To validate this model, we examined changes in T cell gene expression, protein expression and function in Em-TCL1 transgenic mice as they developed CLL 2,3 and demonstrate that development of CLL in these transgenic mice is associated with changes in impaired T cell function and in gene expression in CD4 and CD8 T cells similar to those observed in patients with this disease. Infusion of CLL cells into non-leukemia bearing Em-TCL1 mice rapidly induces these changes, demonstrating a causal relationship between leukemia and the induction of T cell changes. This model allows dissection of the molecular changes induced in CD4 and CD8 T cells by interaction with leukemia cells and further supports the concept that cancer results in complex abnormalities in the immune microenvironment.

Publication Title

E(mu)-TCL1 mice represent a model for immunotherapeutic reversal of chronic lymphocytic leukemia-induced T-cell dysfunction.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE14924
Characterisation of gene expression changes in T cells from patients presenting with AML compared with healthy T cells
  • organism-icon Homo sapiens
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Work previously published by our group has demonstrated that T cells from patients with chronic lymphocytic leukaemia (CLL) show differentially regulated genes compared with healthy T cells. This study was initiated to examine if these gene expression changes were unique to CLL T cells or common to an alternative leukaemia, acute myeloid leukaemia (AML).

Publication Title

Peripheral blood T cells in acute myeloid leukemia (AML) patients at diagnosis have abnormal phenotype and genotype and form defective immune synapses with AML blasts.

Sample Metadata Fields

Sex, Age

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accession-icon GSE33246
Gene Regulation of Intestinal Porcine Epithelial Cells IPECJ2 is Dependent on the Site of Deoxynivalenol Toxicological Action
  • organism-icon Sus scrofa
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Porcine Genome Array (porcine)

Description

Here we analysed different mechanisms of apical and basolateral deoxynivalenol (DON) toxicity reflected in the gene expression.

Publication Title

Gene regulation of intestinal porcine epithelial cells IPEC-J2 is dependent on the site of deoxynivalenol toxicological action.

Sample Metadata Fields

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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