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GSE36057
Mus musculus
5 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Natural Helper cells constitute a unique lineage of Th2-cytokine producting innate lymphocytes, here we characterize the gene expression profile of non-stimulated or PMA/ionomycin-stimulated Natural Helper cells from naive C57Bl/6 mouse lungs.
Publication Title
Lung natural helper cells are a critical source of Th2 cell-type cytokines in protease allergen-induced airway inflammation.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 9 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
FGFR2 risk SNPs confer breast cancer risk by augmenting oestrogen responsiveness.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 5 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Genome-wide association studies have identified a locus within the second intron of the FGFR2 gene that is consistently the most strongly associated with estrogen receptor-poisive breast cancer risk. However, we know little about the mechanisms by which the FGFR2 locus mediates risk or the pathways in which multiple risk loci may combine to cause disease. Previously, a systems biology approach was adopted to elucidate the regulatory networks operating in MCF-7 breast cancer cells in order to examine the role of FGFR2 in mediating risk. Here, the same approach has been employed using MCF-7 cells that have been treated with siRNA directed against FGFR2, in order to knock-down FGFR2 expression, to confirm that the differential gene expression that we see when FGF10 signalling is perturbed, on a background of estrogen signalling, is mediated via FGFR2 stimulation.
Publication Title
FGFR2 risk SNPs confer breast cancer risk by augmenting oestrogen responsiveness.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 70 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The primary goal of toxicology and safety testing is to identify agents that have the potential to cause adverse effects in humans. Unfortunately, many of these tests have not changed significantly in the past 30 years and most are inefficient, costly, and rely heavily on the use of animals. The rodent cancer bioassay is one of these safety tests and was originally established as a screen to identify potential carcinogens that would be further analyzed in human epidemiological studies. Today, the rodent cancer bioassay has evolved into the primary means to determine the carcinogenic potential of a chemical and generate quantitative information on dose-response behavior in chemical risk assessments. Due to the resource-intensive nature of these studies, each bioassay costs $2 to $4 million and takes over three years to complete. Over the past 30 years, only 1,468 chemicals have been tested in a rodent cancer bioassay. By comparison, approximately 9,000 chemicals are used by industry in quantities greater than 10,000 lbs and nearly 90,000 chemicals have been inventoried by the U.S. Environmental Protection Agency as part of the Toxic Substances Control Act. Given the disparity between the number of chemicals tested in a rodent cancer bioassay and the number of chemicals used by industry, a more efficient and economical system of identifying chemical carcinogens needs to be developed.
Publication Title
Application of genomic biomarkers to predict increased lung tumor incidence in 2-year rodent cancer bioassays.
Sample Metadata Fields
Sex, Age, Subject
View Samples- Homo sapiens
- 4 Downloadable Samples
Illumina HiSeq 2000
Description
The capacity of cancer cells to undergo epithelial mesenchymal trans-differentiation has been implicated as a factor driving metastasis, through the acquisition of enhanced migratory/invasive cell programs and the engagement of anti-apoptotic mechanisms promoting drug and radiation resistance. Our aim was to define molecular signaling changes associated with mesenchymal trans-differentiation in two KRas mutant NSCLC models. We focused on central transcription and epigenetic regulators predicted to be important for mesenchymal cell survival. Overall design: Haley, J.A., Haughney, E., Ullman, E., Bean, J., Haley, J.D.* and Fink, M.Y. (2014) 'Altered Transcriptional Control Networks with Trans-Differentiation of Isogenic Mutant KRas NSCLC Models' Front. Oncology, doi/10.3389/fonc.2014.00344.
Publication Title
Altered Transcriptional Control Networks with Trans-Differentiation of Isogenic Mutant-KRas NSCLC Models.
Sample Metadata Fields
Treatment, Subject
View Samples- Mus musculus
- 3 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
In contrast to the migration of leukocytes from blood vessels into tissues, and the involvement of adhesion molecules and chemokines in this process, the migration of leukocytes from the tissue into lymphatic vessels is much less well understood. This can, in part be explained by the fact that murine lymphatic endothelial cells (LECs) have proven particularly hard to isolate and propagate in culture. Hence, it has been difficult to establish suitable models to study this process in vitro. Combining magnetic bead-based purification and fluorescence-activated cell sorting (FACS), we have isolated LECs (immorto-LECs) from the skin of mice which express a temperature-sensitive SV40 large T antigen (H-2Kb-tsA58 mice; ImmortoMice) in all cell types under the control of the MHC-class-I-promotor, H-2Kb. The isolated cells are viable for more than 30 passages when cultured at 33 C, the temperature at which the large T antigen is stably expressed. Furthermore, immorto-LECs tolerate several days of culture at 37 C, but become senescent if continuously cultured at this temperature. All cells stably express endothelial and lymphatic markers like CD31, podoplanin, Prox-1 and VEGFR-3 up to passage 30. When cultured in presence of tumor necrosis factor-alpha (TNF-a), immorto-LECs upregulate adhesion molecules, such as ICAM-1, VCAM-1 and E-selectin, similarly to what has been reported to occur under inflammatory conditions in vivo. Overall, our findings establish immorto-LECs as a useful and handy tool for the in vitro investigation of immune cell transmigration across lymphatic endothelium.
Publication Title
Tissue inflammation modulates gene expression of lymphatic endothelial cells and dendritic cell migration in a stimulus-dependent manner.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 32 Downloadable Samples
- NextSeq 500
Description
Polycomb repressive complex-2 (PRC2) is a group of proteins that play important role during development and in cell differentiation. PRC2 is a histone-modifying complex that catalyses methylation of lysine 27 of histone H3 (H3K27me3) at differentiation genes leading to their transcriptional repression. JARID2 is a co-factor of PRC2 and is important for targeting PRC2 to chromatin as well as modulating its activity. Here, we show that in many human cells, including human epidermal keratinocytes, JARID2 predominantly exists as a novel low molecular weight form, which lacks the N-terminal PRC2-interacting domain (?N-JARID2). We show that ?N-JARID2 is a cleaved product of full-length JARID2 spanning the C-terminal conserved region consisting of jumonji domains. JARID2 knockout in keratinocytes results in up-regulation of cell cycle genes and repression of many epidermal differentiation genes. Surprisingly, repression of epidermal differentiation genes in JARID2-null keratinocytes can be relieved by expression of ?N-JARID2 suggesting that this form promotes activation of these genes and has opposing function to that of PRC2 in regulation of differentiation. We propose that a switch from expression of full-length JARID2 to ?N-JARID2 is important for the up-regulation of genes during differentiation. Overall design: RNA-seq analysis of Wildtype and JARID2-null keratinocytes (HaCaTs) on day 0 and day 3 of calcium induced differentiation.
Publication Title
A novel form of JARID2 is required for differentiation in lineage-committed cells.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 25 Downloadable Samples
- Illumina human-6 v2.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
5-hydroxymethylcytosine marks promoters in colon that resist DNA hypermethylation in cancer.
Sample Metadata Fields
Sex, Specimen part, Cell line, Treatment, Subject
View Samples- Homo sapiens
- 25 Downloadable Samples
- Illumina human-6 v2.0 expression beadchip
Description
The discovery of cytosine hydroxymethylation (5-hmC) as a mechanism that potentially controls DNA methylation changes typical of neoplasia prompted us to investigate its behavior in colon cancer. 5-hmC is globally reduced in proliferating cells such as colon tumors and the gut crypt progenitors, from which tumors can arise. Here, we show that colorectal tumors and cancer cells express Ten-Eleven Translocation (TET) transcripts at levels similar to normal tissues. Genome-wide analyses show that promoters marked by 5-hmC in normal tissue, and those identified as TET2 targets in colorectal cancer cells, are resistant to methylation gain in cancer. In vitro studies of TET2 in cancer cells confirm that these promoters are resistant to methylation gain independently of sustained TET2 expression. We also find that a considerable number of the methylation gain-resistant promoters marked by 5-hmC in normal colon overlap with those that are marked with poised bivalent histone modifications in embryonic stem cells. Together our results indicate that promoters that acquire 5-hmC upon normal colon differentiation are innately resistant to neoplastic hypermethylation by mechanisms that do not require high levels of 5-hmC in tumors. Our study highlights the potential of cytosine modifications as biomarkers of cancerous cell proliferation.
Publication Title
5-hydroxymethylcytosine marks promoters in colon that resist DNA hypermethylation in cancer.
Sample Metadata Fields
Sex, Specimen part, Subject
View Samples- Mus musculus
- 26 Downloadable Samples
- Illumina HiSeq 2500
Description
The transcriptomes of FACS-sorted siglec-F+ alveolar macrophages and siglec-f- CD11b+ exudative macrophages from inducible airway GM-CSF over-expressing transgenic mice (DTGM) were compared to non-inducible littermate controls during influenza A virus infection. Overall design: Examination of effect of GM-CSF on airway macrophages during influenza A virus infection
Publication Title
GM-CSF overexpression after influenza a virus infection prevents mortality and moderates M1-like airway monocyte/macrophage polarization.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject
View Samples