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GSE54043
Homo sapiens
10 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Significant recent progress has been made with understanding eosinophilic gastrointestinal disorders (EGIDs) yet most studies have focused on eosinophilic esophagitis (EoE). Herein, we aimed to provide fundamental information about the molecular characteristics of eosinophilic gastritis (EG).
Publication Title
Histologic eosinophilic gastritis is a systemic disorder associated with blood and extragastric eosinophilia, TH2 immunity, and a unique gastric transcriptome.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
3 eosinophilic esophagitis biopsies, cultured and stimulated with IL-13 : each of them was either left unstimulated or stimulated (100ng for 48h)
Publication Title
IL-13 involvement in eosinophilic esophagitis: transcriptome analysis and reversibility with glucocorticoids.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 9 Downloadable Samples
Illumina HiSeq 2500
Description
Experimental IgE-mediated food allergy depends on intestinal anaphylaxis driven by interleukin (IL)-9. However, the primary cellular source of IL-9 and the mechanisms underlying the susceptibility to food-induced intestinal anaphylaxis remain unclear. Herein, we have reported the identification of multifunctional IL-9-producing mucosal mast cells (MMC9s) that can secrete prodigious amounts of IL-9 and IL-13 in response to IL-33, and mast cell protease-1 (MCPt-1) in response to antigen and IgE complex crosslinking, respectively. Repeated intragastric antigen challenge induced MMC9 development that required T cells, IL-4, and STAT6 transcription factor, but not IL-9 signals. Mice ablated of MMC9 induction failed to develop intestinal mastocytosis, which resulted in decreased food allergy symptoms that could be restored by adoptively transferred MMC9s. Finally, atopic patients that developed food allergy displayed increased intestinal expression of Il9 and MC-specific transcripts. Thus, the induction of MMC9s is a pivotal step to acquire the susceptibility to IgE-mediated food allergy. Overall design: dUTP mRNA-Seq profiles of indicated hematopoietic cell lineages were generated on Illumina HiSeq2500. Hematopoietic cells were isolated from Balb/C mice that developed food allergy and bone marrow-derived mast cells were generated from naïve Balb/C mice
Publication Title
Induction of Interleukin-9-Producing Mucosal Mast Cells Promotes Susceptibility to IgE-Mediated Experimental Food Allergy.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Small intestine of a pool of three Wt mice and a pool of 3 IL-9tg mice in a balb/c backround.
Publication Title
IL-9- and mast cell-mediated intestinal permeability predisposes to oral antigen hypersensitivity.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2000
Description
Mouse Embryonic Stem Cells (ESCs) express PDGFRa heterogeneously, fluctuating between a PDGFRa+ (PrE-primed) and a Platelet Endothelial Cell Adhesion Molecule 1 (PECAM1)-positive state (epiblast-primed). The two surface markers can be co-detected on a third subpopulation, expressing epiblast and PrE determinants. Overall design: Three different subpopulatiosn were sorted based on PECAM1/PDGFRa expression and analyzed by NGS
Publication Title
PDGFRα<sup>+</sup> Cells in Embryonic Stem Cell Cultures Represent the In Vitro Equivalent of the Pre-implantation Primitive Endoderm Precursors.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 14 Downloadable Samples
Description
Major roadblocks to developing effective progesterone receptor (PR)-targeted therapies in breast cancer include the lack of highly-specific PR modulators, a poor understanding of the pro- or anti-tumorigenic networks for PR isoforms and ligands, and an incomplete understanding of the cross talk between PR and estrogen receptor (ER) signaling. Through genomic analyses of xenografts treated with various clinically-relevant ER and PR-targeting drugs, we describe how the activation or inhibition of PR dictates distinct ER and PR chromatin binding and differentially reprograms estrogen signaling, resulting in the segregation of transcriptomes into separate PR agonist and antagonist-mediated groups. These findings address an ongoing controversy regarding the clinical utility of PR agonists and antagonists, alone or in combination with tamoxifen, for breast cancer management. Genomic analyses of the two PR isoforms, PRA and PRB, indicate that these isoforms bind distinct genomic sites and interact with different sets of co-regulators to differentially modulate gene expression as well as pro- or anti-tumorigenic phenotypes. Of the two isoforms, PRA inhibited gene expression and ER chromatin binding significantly more than PRB. Of note, the two isoforms reprogrammed estrogen activity to be either pro or anti-tumorigenic. In concordance to the in-vitro observations, differential gene expression was observed in PRA and PRB-rich patient tumors and importantly, PRA-rich gene signatures had poorer survival outcomes. In support of antiprogestin responsiveness of PRA-rich tumors, gene signatures associated with PR antagonists, but not PR agonists, predicted better survival outcomes. This differential of better patient survival associated with PR antagonists versus PR agonists treatments was further reflected in the higher anti-tumor activity of combination therapies of tamoxifen with PR antagonists and modulators. Knowledge of various determinants of PR action and their interactions with estrogen signaling to differentially modulate breast cancer biology should serve as a guide to the development of biomarkers for patient selection and translation of PR-targeted therapies to the clinic. Overall design: For in-vitro experiments, cells were grown in steroid-deprived RPMI for 48 hours to 80% confluence, before being treated for with the hormones of interest (vehicle, 10 nM estrogen, 10 nM R5020 or both estrogen +R5020). Cells were then fixed with 1% formaldehyde for 10 minutes and the crosslinking was quenched with 0.125 M glycine for 5 minutes. Fixed cells were suspended in ChIP lysis buffer (1 ml 1M Tris pH 8.0; 200 µl 5M NaCl; 1 ml 0.5M EDTA; 1 ml NP-40; 1 g SDS, 0.5 g deoxycholate) and sheared in the Diagenode Biorupter for 20 minutes (30 second cycles). 100 µl of sheared chromatin was removed as input control. A 1:10 dilution of sheared chromatin in ChIP dilution buffer (1.7 ml 1M Tris pH 8.0; 3.3 ml 5M NaCl; 5 ml 10% NP-40; 200 µl 10% SDS; to 100 ml with H2O), 4 µg antibody and 30 µl magnetic DynaBeads were incubated in a rotator at 4oC overnight. Chromatin was immunoprecipitated overnight using anti-ER (Santa Cruz Biotechnology HC-20), anti-PR (in-house made KD68) or rabbit IgG (Santa Cruz Biotechnology SC-2027). Next, the immunoprecipitated chromatin was washed with ChIP wash buffer I (2 ml 1M Tris pH 8.0; 3 ml 5M NaCl; 400 µl 0.5M EDTA; 10 ml 10% NP-40; 1 ml 10% SDS; to 100 ml with H2O), ChIP wash buffer II (2 ml 1M Tris pH 8.0; 10 ml 5M NaCl; 400 µl 0.5M EDTA; 10 ml 10% NP-40; 1 ml 10% SDS; to 100 ml with H2O), ChIP wash buffer III (1 ml 1M Tris pH 8.0; 5 ml of 5M LiCl; 200 µl 0.5M EDTA; 10 ml 10% NP-40; 10 ml 10% deoxycholate; to 100 ml with H2O) and TE (pH 8.0). Elution was performed twice from beads by incubating them with 100 µl ChIP-elution buffer (1% SDS, 0.1 M NaHCO3) at 65oC for 15 minutes each. The eluted protein-DNA complexes were de-crosslinked overnight at 65oC in 200 µM NaCl. After de-crosslinking, the mixture was treated with proteinase K for 45 minutes followed by incubation with RNase A for 30 minutes. Finally, DNA fragments were purified using Qiagen PCR purification kit and reconstituted in 50 µl nuclear-free water. Real time PCR was performed using SYBR green. For ChIP-seq library preparations, libraries were prepared using KapaBiosystems LTP library preparation kit (#KK8232) according to the manufacturer's protocol.
Publication Title
Progesterone receptor isoforms, agonists and antagonists differentially reprogram estrogen signaling.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina HiSeq 2500
Description
In this study we determine the transcriptional profile by RNAseq of mESC in the absence of Smad1 and Smad5 and in subpopulation of mESC with different levels of BMP-SMAD activation. Overall design: Transcriptome analysis using RNAseq was performed on 3 biological replicates of BRE negative and positive mESC subpopulations, which were collected in pairs at 3 different times. Transcriptome analysis using RNAseq was performed on Smad1/5 floxed (FL) and knockout (KO) mESC. Two different parental cell lines were used. For each parental cell line we analyzed one Smad1/5 FL sample and two Smad1/5 KO samples, resulting in respectively two and four biological replicates for the FL and KO conditions.
Publication Title
BMP-SMAD Signaling Regulates Lineage Priming, but Is Dispensable for Self-Renewal in Mouse Embryonic Stem Cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Saccharomyces cerevisiae
- 8 Downloadable Samples
- Affymetrix Yeast Genome S98 Array (ygs98)
Description
In Saccharomyces cerevisiae, the maturation of both pre-rRNA and pre-small nucleolar RNAs (pre-snoRNAs) involves common factors, thereby providing a potential mechanism for the coregulation of snoRNA and rRNA synthesis. In this study, we examined the global impact of the double-stranded-RNA-specific RNase Rnt1p, which is required for pre-rRNA processing, on the maturation of all known snoRNAs. In silico searches for Rnt1p cleavage signals, and genome-wide analysis of the Rnt1p-dependent expression profile, identified seven new Rnt1p substrates. Interestingly, two of the newly identified Rnt1p-dependent snoRNAs, snR39 and snR59, are located in the introns of the ribosomal protein genes RPL7A and RPL7B. In vitro and in vivo experiments indicated that snR39 is normally processed from the lariat of RPL7A, suggesting that the expressions of RPL7A and snR39 are linked. In contrast, snR59 is produced by a direct cleavage of the RPL7B pre-mRNA, indicating that a single pre-mRNA transcript cannot be spliced to produce a mature RPL7B mRNA and processed by Rnt1p to produce a mature snR59 simultaneously. The results presented here reveal a new role of yeast RNase III in the processing of intron-encoded snoRNAs that permits independent regulation of the host mRNA and its associated snoRNA.
Publication Title
Genome-wide prediction and analysis of yeast RNase III-dependent snoRNA processing signals.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 54 Downloadable Samples
- NextSeq 500
Description
Transcriptionally similar subpopulations of exhausted CD8+ T-cells are found in chronic viral infection and tumors Overall design: RNA-seq analysis of progenitor exhausted and terminally exhausted CD8+ T-cells isolated from spleens of mice chronically infected with LCMV Clone 13 (day 30 post-infection) or isolated from B16-ova tumors (day 22 post tumor implantation), with or without anti-PD-1 treatment
Publication Title
Subsets of exhausted CD8<sup>+</sup> T cells differentially mediate tumor control and respond to checkpoint blockade.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 4 Downloadable Samples
- NextSeq 500
Description
Distinct populations of progenitor exhausted (Tcf1+Tim-3-) and terminally exhausted (Tcf1-Tim-3+) CD8+ T-cells occur in B16-OVA tumors Overall design: Profiling of CD8+ T-cells from day 10 and day 20 B16-OVA mouse melanoma tumors
Publication Title
Subsets of exhausted CD8<sup>+</sup> T cells differentially mediate tumor control and respond to checkpoint blockade.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples