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accession-icon GSE34206
Gene regulation in macrophages from irradiated tumors
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Tumors engender an environment dominated by M2 differentiated tumor macrophages that support tumor invasion, metastases and escape from immune control. In this study, we demonstrate that following radiation therapy of tumors in mice there is an influx of tumor macrophages that polarize towards wound repair and immune suppression.

Publication Title

Expression of NF-κB p50 in tumor stroma limits the control of tumors by radiation therapy.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE46036
Escalating-dose peptide immunotherapy induces progressive immunoregulatory changes in self-reactive T cells
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Peptide immunotherapy aims to specifically restore tolerance to the administered self-antigen and prevent autoimmunity without the perturbation of normal immune function. We have developed a dose escalation protocol for subcutaneous delivery of the MHC II-restricted myelin basic protein peptide analogue Ac1-9[4Y] to T cell receptor transgenic (Tg4) mice. Dose escalation allows safe administration of high doses of peptide, which effectively induces antigen-specific tolerance and suppresses the development of experimental autoimmune encephalomyelitis, a model for the human condition multiple sclerosis. CD4+ T cells isolated from treated mice are anergic and suppressive in vitro and respond to stimulation by secretion of the immunoregulatory cytokine IL-10. To understand the molecular changes occurring throughout the course of dose-escalation immunotherapy, we undertook microarray analysis of CD4+ T cells at different the stages of treatment, using Tg4 Rag-1 deficient mice, which lack naturally occurring regulatory T cells and have a monoclonal CD4+ T cell population

Publication Title

Sequential transcriptional changes dictate safe and effective antigen-specific immunotherapy.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP064595
RNA-seq analysis of LPS induced RIPK1 kinase dependent gene expression changes in CD11b+ myeloid bone marrow cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We used RNA-seq as a method of next generation sequencing (NGS) to identify RIPK1 dependent inflammatory mediators and pathways in LPS injected mice. Overall design: Mice were divided intro 3 groups - control (n=2), LPS (n=2) and LPS/Nec-1 (n=2). BM cells were isolated by FACS as described for qPCR analysis. Total RNAs were isolated using Qiagen RNeasy kit according to the manufacturer's protocol

Publication Title

RIPK1 and RIPK3 Kinases Promote Cell-Death-Independent Inflammation by Toll-like Receptor 4.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon GSE72797
Genome wide Affymetric Microarray analysis for RIPK1 dependent inflammatory changes in Bone Marrow Derived Macrophages (BMDMs)
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Gene level expression estimate using the Whole Transcript (WT) Assay approach of the Gene 1.0 ST Array System for Mouse. This assay was done to identify the RIPK1-dependent gene expression changes in mouse BMDMs.

Publication Title

RIPK1 and RIPK3 Kinases Promote Cell-Death-Independent Inflammation by Toll-like Receptor 4.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE84142
Effect of Serum Response Factor (SRF) gene deletion on the adult cardiac gene expression at baseline and in response to phenylephrine
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The objective of this study is to assess the effects of the Serum Response Factor deletion on the cardiac gene expression program at different time points after the deletion (day 8 and day 25) and to compare the response of SRF-deficient heart and control heart to phenylephrine, an alpha-adrenergic agonist triggering cardiac hypertrophy.

Publication Title

Nicotinamide Riboside Preserves Cardiac Function in a Mouse Model of Dilated Cardiomyopathy.

Sample Metadata Fields

Sex

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accession-icon GSE104394
The Tumor Suppressor Hic1 Maintains Chromosomal Stability Independent of Tp53
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The tumor suppressor Hic1 maintains chromosomal stability independent of Tp53.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE104392
Analysis of gene expression in control, Hic1 KO and p53 KO mouse embrynoic fibroblast (MEF) cell lines I
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

We hypothesised that genetic inactivation of the transcriptional repressor Hic1, would lead to changes in gene expression that may lead to transformation. We assessed changes in gene expression in pre-immortal MEF cell lines in which Hic1 was inactivated compared to controls.

Publication Title

The tumor suppressor Hic1 maintains chromosomal stability independent of Tp53.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE104393
Analysis of gene expression in control, Hic1 KO and p53 KO mouse embrynoic fibroblast (MEF) cell lines II
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

We hypothesised that genetic inactivation of the transcriptional repressor Hic1, would lead to changes in gene expression that may lead to transformation. We assessed changes in gene expression in immortal MEF cell lines in which Hic1 or p53 was inactivated.

Publication Title

The tumor suppressor Hic1 maintains chromosomal stability independent of Tp53.

Sample Metadata Fields

No sample metadata fields

View Samples
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 GSE25541
cAMP/PKA signaling balances respiratory activity with mitochondria dependent apoptosis via transcriptional regulation
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

This data provides evidence that elevation of cAMP levels has a dramatic effect on the transcriptome of yeast cells, with particular emphasis on mitochondrial function and the promotion of ROS production

Publication Title

cAMP/PKA signaling balances respiratory activity with mitochondria dependent apoptosis via transcriptional regulation.

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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