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.
Expression of NF-κB p50 in tumor stroma limits the control of tumors by radiation therapy.
Specimen part, Treatment, Time
View SamplesPeptide 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
Sequential transcriptional changes dictate safe and effective antigen-specific immunotherapy.
Specimen part, Treatment
View SamplesWe 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
RIPK1 and RIPK3 Kinases Promote Cell-Death-Independent Inflammation by Toll-like Receptor 4.
Specimen part, Cell line, Treatment, Subject
View SamplesGene 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.
RIPK1 and RIPK3 Kinases Promote Cell-Death-Independent Inflammation by Toll-like Receptor 4.
Sex, Specimen part
View SamplesThe 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.
Nicotinamide Riboside Preserves Cardiac Function in a Mouse Model of Dilated Cardiomyopathy.
Sex
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The tumor suppressor Hic1 maintains chromosomal stability independent of Tp53.
No sample metadata fields
View SamplesWe 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.
The tumor suppressor Hic1 maintains chromosomal stability independent of Tp53.
No sample metadata fields
View SamplesWe 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.
The tumor suppressor Hic1 maintains chromosomal stability independent of Tp53.
No sample metadata fields
View SamplesGlucosamine 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.
Exogenous glucosamine globally protects chondrocytes from the arthritogenic effects of IL-1beta.
Age
View SamplesThis 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
cAMP/PKA signaling balances respiratory activity with mitochondria dependent apoptosis via transcriptional regulation.
Treatment
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