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GSE39539
Mus musculus
9 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
A suggested role for fibrillr collagen topology in the pregnancy-induced protection and invasive phenotype.
Publication Title
Collagen architecture in pregnancy-induced protection from breast cancer.
Sample Metadata Fields
Cell line
View Samples- Saccharomyces cerevisiae
- 4 Downloadable Samples
Illumina HiSeq 2000, Illumina Genome Analyzer IIx
Description
Data for replicate Drn1-TAP and Dbr1-TAP CLIP-seq experiments to identify RNA-protein interactions Overall design: Drn1-TAP and Dbr1-TAP CLIP-seq
Publication Title
A homolog of lariat-debranching enzyme modulates turnover of branched RNA.
Sample Metadata Fields
Disease, Subject
View Samples- Homo sapiens
- 33 Downloadable Samples
- Illumina HiSeq 2500
Description
The goal of this study was to define relationships between peripheral blood miRNAs and mRNAs of women undergoing idiopathic preterm labor (PTL) and compare network level changes to control women that deliver at term.Using RNA Sequencing we have performed global miRNA and mRNA profiling in both monocytes and whole blood leukocytes of women who underwent PTL (N=15) matched to non-pathological controls (N=30) as a part of the Ontario Birth Study cohort. We have identified differentially expressed miRNAs, mRNAs and pathways associated with PTL. Intriguingly, we found perturbations in many cellular signaling pathways, particularly in interleukin signaling. We also predicted mRNA targets for specific miRNAs and used these predictions to build putative miRNA-mRNA networks. We identified 6 miRNAs significantly associated with PTL whose expression is negatively correlated with expression of 14 predicted mRNA targets that are also significantly associated with PTL. Overall design: miRNA and mRNA were quantified from whole blood and monocytes of women undergoing spontaneous preterm labor compared to nonlabor controls matched on gestational age
Publication Title
Comparative analysis of gene expression in maternal peripheral blood and monocytes during spontaneous preterm labor.
Sample Metadata Fields
Subject
View Samples- Arabidopsis thaliana
- 12 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Microarray expression profiling was used to identify genes expressed misexpressed in wild-type Arabidopsis seedlings treated with 5-aza-2 deoxyctidine (5AC) or trichostatin A (TSA), and in decrease in dna methylation1 (ddm1) mutant seedlings.
Publication Title
Changes in global gene expression in response to chemical and genetic perturbation of chromatin structure.
Sample Metadata Fields
Specimen part
View Samples- Drosophila melanogaster
- 8 Downloadable Samples
- Illumina HiSeq 2000
Description
Biological systems display extraordinary robustness. Robustness of transcriptional enhancers results mainly from clusters of binding sites for the same transcription factor, and it is not clear how robust enhancers can evolve loss of expression through point mutations. Here, we report the high-resolution functional dissection of a robust enhancer of the shavenbaby gene that has contributed to morphological evolution. We found that robustness is encoded by many binding sites for the transcriptional activator Arrowhead and that, during evolution, some of these activator sites were lost, weakening enhancer activity. Complete silencing of enhancer function, however, required evolution of a binding site for the spatially restricted potent repressor Abrupt. These findings illustrate that recruitment of repressor binding sites can overcome enhancer robustness and may minimize pleiotropic consequences of enhancer evolution. Recruitment of repression may be a general mode of evolution to break robust regulatory linkages. Overall design: 8 samples are analyzed: background GFP- and target GFP+ cells from four independent sortings.
Publication Title
Evolved Repression Overcomes Enhancer Robustness.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Illumina HiSeq 4000
Description
Pdgfra-expressing (Pdgfra+) cells have been implicated as progenitors in many mesenchymal tissues. To further characterize Pdgfra+ cells during alveologensis, we performed single-cell RNA sequencing (scRNA-Seq) analysis using fluorescence-activated cell sorting (FACS) sorted GFP+ cells from Pdgfra-GFP lungs at P7 and P15. Overall design: We perfomed 10X genomics single-cell RNA-seq of Pdgfra-GFP+ cells at P7 and P15
Publication Title
<i>Pdgfra</i> marks a cellular lineage with distinct contributions to myofibroblasts in lung maturation and injury response.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 143 Downloadable Samples
- Illumina HiSeq 2500, Illumina HiSeq 2000
Description
Cancer-associated inflammatory processes in the tumour microenvironment, as well as systemically, are strongly linked with poor disease outcome in cancer patients. For most human solid tumour types, high systemic neutrophil-to-lymphocyte ratios (NLR) are associated with increased metastasis and poor overall survival and recent experimental studies have demonstrated a causal relationship between neutrophils and metastasis formation. However, to date, the cancer cell-intrinsic mechanisms dictating the substantial heterogeneity in systemic neutrophilic inflammation between tumour-bearing hosts are largely unresolved. Using a panel of 16 distinct genetically engineered mouse models (GEMMs) for breast cancer, we demonstrate that tumour cell-intrinsic loss of p53 changes the phenotype and function of macrophages in the microenvironment, leading to activation of a systemic inflammatory cascade that drives neutrophil expansion. Mechanistically, p53 loss in cancer cells induces secretion of Wnt ligands that act in a paracrine fashion to stimulate IL-1b production from tumour-associated macrophages. Intratumoural IL-1ß production stimulates an inflammatory cascade leading to the systemic accumulation of neutrophils. Pharmacological and genetic blockade of cancer cell-derived Wnt secretion reverses IL-1ß expression by macrophages and subsequent systemic neutrophilic inflammation. Collectively, using pre-clinical mouse models for breast cancer, we demonstrate a novel mechanistic link between loss of p53 in cancer cells, Wnt ligand secretion and systemic immune activation. This illustrates the importance of cancer cell-intrinsic genetic aberrations in dictating cancer-associated inflammation. These insights set the stage for personalized immune intervention strategies for cancer patients. Overall design: In this study, gene expression profiles of tumours from genetically engineered mouse models (GEMMs) were analysed using RNA sequencing. Analysis was performed on bulk tumours of 10 GEMMs with different tissue-specific mutations driving tumorigenesis, totalling to 125 different tumours (n=5 or more per group). Subsequently, samples were grouped according to p53 status of the tumour (models containing Trp53 floxed alleles, or not) and comparisons were made between p53-KO and p53-WT tumours.
Publication Title
Loss of p53 triggers WNT-dependent systemic inflammation to drive breast cancer metastasis.
Sample Metadata Fields
Cell line, Subject
View Samples- Macaca mulatta, Pan troglodytes, Homo sapiens
- 29 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Divergent whole-genome methylation maps of human and chimpanzee brains reveal epigenetic basis of human regulatory evolution.
Sample Metadata Fields
No sample metadata fields
View Samples- Macaca mulatta, Pan troglodytes, Homo sapiens
- 29 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We identified human-specific gene expression patterns in the brain by comparing expression with chimpanzee and rhesus macaque
Publication Title
Divergent whole-genome methylation maps of human and chimpanzee brains reveal epigenetic basis of human regulatory evolution.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Glucose is the most important metabolic substrate of the retina and maintenance of nor-moglycemia is an essential challenge for diabetic patients. Glycemic excursions could lead to cardiovascular disease, nephropathy, neuropathy and retinopathy. We recently showed that hy-poglycemia induced retinal cell death in mouse via caspase 3 activation and glutathione (GSH) decrease. Ex vivo experiments in 661W photoreceptor cells confirmed the low-glucose induction of death via superoxide production and activation of caspase 3, which was concomitant with a decrease of GSH content. We evaluate herein retinal gene expression 4 h and 48 h after insulin-induced hypoglycemia. Microarray analysis demonstrated clusters of genes whose expression is modified by hypoglycemia and we discuss the potential implication of those genes in retinal cell death. In addition, we highlight, by gene set enrichment analysis, three important pathways, including KEGG lysosomes, KEGG GSH metabolism and REACTOME apoptosis pathways. We tested the effect of recurrent hypoglycemia (three successive 5h periods of hypoglycemia separated by 48 h recovery) on retinal cell death. Interestingly, exposure to multiple hypoglycemic events prevents retinal cell death and GSH decrease, or adapts the retina to external stress by restoring GSH level comparable to control situation. We hypothesize that scavenger GSH is a key compound in this apoptotic process, and maintaining normal GSH level, as well as a strict glycemic control, may represent a therapeutic challenge in order to avoid side effects of diabetes, especially diabetic retinopathy.
Publication Title
Biological Characterization of Gene Response to Insulin-Induced Hypoglycemia in Mouse Retina.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples