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accession-icon SRP071332
Expression profiling of IL-13 stimulated PBMCs with and without an IL-13R antagonist
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

This experiment aims to identify the biological pathways and diseases associated with the cytokine Interleukin 13 (IL-13) using gene expression measured in peripheral blood mononuclear cells (PBMCs). Overall design: The experiment comprised of samples obtained from 3 healthy donors. The expression profiles of in vitro IL-13 stimulation were generated using RNA-seq technology for 3 PBMC samples at 24 hours. The transcriptional profiles of PBMCs without IL-13 stimulation were also generated to be used as controls. An IL-13R-alpha antagonist (Redpath et al. Biochemical Journal, 2013) was introduced into IL-13 stimulated PBMCs and the gene expression levels after 24h were profiled to examine the neutralization of IL-13 signaling by the antagonist.

Publication Title

Combining multiple tools outperforms individual methods in gene set enrichment analyses.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP163432
Genomic Reorganization of Lamin-Associated Domains in Cardiac Myocytes is Associated with Differential Gene Expression and DNA Methylation in Human Dilated Cardiomyopathy [RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Mutations in the LMNA gene causes set of disorders collectively referred to as laminopathies that include dilated cardiomyopathy. Lamin A/C proteins a components of nuclear lamina forms distinct nuclear domains called lamina associated domains (LADs). The roles of LADs in DCM is not known. To identify LADs and characterize their associations with CpG methylation and gene expression in human cardiac myocytes isolated from patients with DCM and controls we performed Chromatin immunoprecipitation-sequencing (ChIP-Seq), reduced representative bisulfite sequencing (RRBS), and RNA-sequencing (RNA-Seq) in 5 control and 5 DCM hearts with defined pathogenic variants in the LMNA gene. LADs are redistributed in DCM, are associated with CpG methylation and suppressed transcription, contributing to the pathogenesis of DCM in laminopathies. Overall design: integrated analysis of ChIP-seq for LMNA from Cardiac myocytes and RNA-seq and RRBS from 5 control and 5 DCM human heart sample

Publication Title

Genomic Reorganization of Lamin-Associated Domains in Cardiac Myocytes Is Associated With Differential Gene Expression and DNA Methylation in Human Dilated Cardiomyopathy.

Sample Metadata Fields

Sex, Age, Subject

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accession-icon GSE20437
Histologically normal epithelium from breast cancer patients and cancer-free prophylactic mastectomy patients
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Gene expression in histologically normal epithelium from breast cancer patients and cancer-free prophylactic mastectomy patients share a similar profile

Publication Title

Gene expression in histologically normal epithelium from breast cancer patients and from cancer-free prophylactic mastectomy patients shares a similar profile.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE46534
Development of MLL-rearranged leukemia is dependent on a transcriptional program orchestradt by C/EBP
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Translocations involving the MLL genes are frequently found in Acute Myeloid Leukemia (AML) and are associated with poor prognosis. The MLL fusion proteins act as aberrant transcription factor activating a transcriptional program that transforms the cells, potentially through collaboration with other transcription factors. To investigate this we searched gene expression profiles from patients with MLL-rearranged AML compared with normal hematopoietic progenitor cells for transcriptional regulators and found targets of C/EBP to be up-regulated in the AML samples, suggesting that C/EBP might collaborate with MLL fusion proteins in the initial transformation process. We could show that transformation by MLL fusion proteins is dependent on C/EBP activity both in early progenitors as well as in GMPs. In contrast, C/EBP was found to be indispensable in an already established leukemia. These results suggest that C/EBP play an important role in the early transforming event of leukemogenesis.

Publication Title

Initiation of MLL-rearranged AML is dependent on C/EBPα.

Sample Metadata Fields

Specimen part

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accession-icon GSE15723
Gene profile in H1299 cells treated with PTD-DRBD GAPDH siRNA or treated with Lipofection GAPDH siRNA
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina human-6 v2.0 expression beadchip

Description

Whole genome microarrays were probed with total mRNA from PTD-DRBD GAPDH siRNA treated H1299 cells at 12 h and 24 h. Using a 1.6x fold increase/decrease filter of cellular mRNAs, we detected a dramatic reduction in the target GAPDH mRNA along with a limited number of both up and down regulated genes. The up regulated genes were reduced in numbers and to nearly background 1.6x levels at 24 h, while the down regulated genes increased slightly in numbers and maintained a similar magnitude at 24 h. In contrast, lipofection treated cells showed both a dramatic increase in both the total number of genes altered and the magnitude of the increase. In addition, the numbers of genes affected increased between 12 h and 24 h, suggesting that lipofection of siRNAs into cells results in a substantial alteration to the transcriptome and may thereby confound interpretation of experimental outcomes. Moreover, the GAPDH specific knockdown was significantly smaller than PTD-DRBD mediated knockdown.

Publication Title

Efficient siRNA delivery into primary cells by a peptide transduction domain-dsRNA binding domain fusion protein.

Sample Metadata Fields

Cell line, Time

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accession-icon GSE55713
TGIF1 is a negative regulator of MLL-rearranged acute myeloid leukemia
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The aim of the study was to investigate the role of TGIF1 in MLL-AF9 transformed cells

Publication Title

TGIF1 is a negative regulator of MLL-rearranged acute myeloid leukemia.

Sample Metadata Fields

Cell line

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accession-icon SRP150419
Haemopedia: Human Haematopoietic Gene Expression
  • organism-icon Homo sapiens
  • sample-icon 84 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Database of gene expression in different haematopoietic cell types at haemosphere.org Overall design: Comparison of gene expression in different haematopoietic cell types

Publication Title

Haemopedia RNA-seq: a database of gene expression during haematopoiesis in mice and humans.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE76966
G-CSF receptor targeting in inflammatory arthritis
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

G-CSF is a hemopoietic growth factor that has a role in steady state granulopoiesis, as well as in mature neutrophil activation and function. We developed a neutralizing monoclonal antibody to the murine G-CSF receptor (G-CSFR), which antagonizes binding of murine G-CSF and inhibits G-CSFR signalling. Anti-G-CSFR rapidly halts the progression of established disease in collagen antibody-induced arthritis (CAbIA). Neutrophil accumulation in joints is inhibited, without rendering animals neutropenic, suggesting an effect on homing to inflammatory sites. Neutrophils in the blood and arthritic joints of anti-G-CSFR treated mice show alterations in cell adhesion receptors, while anti-G-CSFR suppresses local production of proinflammatory cytokines and chemokines known to drive tissue damage. Our aim in this study was to use differential gene expression analysis of joint and blood neutrophils to more thoroughly understand the effect of G-CSFR blockade on the inflammatory response following anti-G-CSFR therapy in CAbIA.

Publication Title

Therapeutic Targeting of the G-CSF Receptor Reduces Neutrophil Trafficking and Joint Inflammation in Antibody-Mediated Inflammatory Arthritis.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage, Treatment

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accession-icon GSE48359
Transcriptomic analysis of midbrain and individual hindbrain rhombomeres in the chick embryo
  • organism-icon Gallus gallus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Chicken Genome Array (chicken)

Description

A systematic survey of the transcriptional status of individual segments of the developing chick hindbrain (r1-5) and the adjacent region of the embryonic midbrain (m) during the HH11 stage of chick development

Publication Title

Transcriptomic analysis of midbrain and individual hindbrain rhombomeres in the chick embryo.

Sample Metadata Fields

Specimen part

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accession-icon GSE72613
Characterization of the SouR regulon in Pseudomonas aeruginosa
  • organism-icon Pseudomonas aeruginosa
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Pseudomonas aeruginosa Array (paeg1a)

Description

The sarcosine oxidase locus is controlled by GbdR and SouR independently induced by glycine betaine and sarcosine, respectively. The goal of this study was to identify the members of the SouR regulon. Therefore, the comparison strains were a gbdR mutant and a gbdRsouR double mutant.

Publication Title

Sarcosine Catabolism in Pseudomonas aeruginosa Is Transcriptionally Regulated by SouR.

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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