E-GEOD-33292
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA149283
PROVIDER: E-GEOD-33292 | ExpressionAtlas | 2015-09-21
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-33292-analysis-methods.tsv | Tabular | |||
| E-GEOD-33292-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-33292-configuration.xml | Xml | |||
| E-GEOD-33292-percentile-ranks.tsv | Tabular | |||
| E-GEOD-33292.condensed-sdrf.tsv | Tabular |
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Project description:Expression data from WT DN3, TCF-1-deficient DN3 thymocytes, and T cell lymphomas in TCF-1-deficient animals.
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Project description:Themis1, a recently described T-lineage specific protein, is essential for thymic positive and negative selection. Although Themis1 has been clearly identified as a component of the T cell antigen receptor (TCR) signalosome, its precise role in TCR signaling remains unclear. Here, we used quantitative proteomic and TCR signaling reporter mice to gain insight into Themis1 signaling function. Mass spectrometry analysis of the Themis1 interactome identified Grb2, SHP1 and Vav1 as the principal interacting partners of Themis1 in thymocytes. The dataset contains mass spectrometry results from the analysis of 6 different kind of AP-MS purifications (based on immunoprecipitation using a Themis1 antibody) starting from the following samples: - thymocytes from WT mice, non stimulated (noted WT NS) - thymocytes from WT mice, stimulated with pervanadate (noted WT P) - thymocytes from GRB2 +/- mice (with decreased expression of GRB2), non stimulated (noted GRB2 NS) - thymocytes from GRB2 +/- mice (with decreased expression of GRB2), stimulated with pervanadate (noted GRB2 P) - thymocytes from Themis1 -/- mice (knock-out for Themis1), non stimulated (noted KO NS) - thymocytes from Themis1 -/- mice (knock-out for Themis1), stimulated with pervanadate (noted KO P) Three biological replicates were prepared for these 6 different conditions (noted, 1,2,3), yielding 18 analyzed samples. Three technical nanoLC-MS runs were acquired for each sample (noted R1, R2, R3), leading to the 54 nanoLC-MS raw files contained in the dataset.
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Project description:Expression data from Thymocytes of WT, TCF-1-deficient and β-catenin transgenic mice
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Project description:To gain a molecular view of E-proteins with respect to the development of Foxp3+ T cells, we perform microarray studies that would identify transcription factors that are up-regulated as E-proteins levels fall and and Foxp3 expression rises. We hypothesize that such transcription factors activate the synthesis of key proteins necessary for the development of Foxp3+ cells in the thymus (or in the periphery). Among the possible proteins (negatively regulated by E-protein are those involved in IL-2 signaling, since the latter has been shown to be critical for the development of Foxp3+ cells in the thymus. In the planned studies we will extract mRNA from sorted Foxp3+GFP+ thymocytes from wild type (WT) mice and similar cells from E-protein deficient thymocytes. However, since Foxp3+ thymocytes in WT mice already have reduced E-protein levels, differences between thymocytes from these mice and E-protein deficient mice might be minimal. We therefore will also extract mRNA from Foxp3-negative thymocytes from WT mice whose E-proteins levels have not fallen sufficient low to allow Foxp3 expression and Foxp3-negative thymocytes from E-protein deficient mice whose E-proteins are necessarily low but have not expressed Foxp3 for unrelated reasons.
2014-12-31 | GSE51654 | GEO
Project description:T cell development is accompanied by epigenetic changes that ensure the silencing of stem cell-related, and the activation of lymphocyte-specific programs. How transcription factors influence these changes remains unclear. We show that the Ikaros transcription factor interacts with the Polycomb Repressive Complex 2 (PRC2) in CD4-CD8- thymocytes, and allows its binding to >200 developmentally-regulated genes, many of which are expressed in hematopoietic stem cells. Loss of Ikaros in CD4-CD8- cells leads to diminished histone H3 Lys27 (H3K27) trimethylation and ectopic expression of these genes. Ikaros binding triggers PRC2 recruitment and H3K27 trimethylation. Furthermore, Ikaros interacts with PRC2 independently of the Nucleosome Remodeling and Deacetylation complex. Our results identify Ikaros as a fundamental regulator of PRC2 function in developing T cells. Genome-wide comparison of different histone modifications, Ikaros, Suz12 and NuRD binding in different stages of T cell development in WT and Ikaros mutant mice. Profiling of H3K27me3 in DN1, DN2, DN3, DN4 and DP thymocytes and hematopoietic stem and progenitor cells (LSK cells) of WT and Ikaros mutant mice. Profiling of H3K4me3 and H3ac in WT and Ikaros mutant DP thymocytes. Global analysis of Ikaros binding in WT DN3, DN4 and DP cells, Suz12 binding in WT and Ikaros mutant DN3 cells, and Mta2 and Mi2beta binding in WT DN3 cells. Genome-wide profiling of Ikaros binding and H3K27me3 upon Ikaros activation in Ikaros-deficient leukemic T cells.
2015-11-03 | E-GEOD-61148 | biostudies-arrayexpress
Project description:Both TCF-1 and its coactivator β-catenin are known to be required for supporting normal double positive (DP) thymocyte survival through upregulating Bcl-xL. However, the downstream factors mediating this effect remained unknown. We used microarray to compare the global expression difference among WT, TCF-1-deficient, and β-catenin transgenic thymocytes to search for the genes that are down-regulated and up-regulated in TCF-1-deficient and β-catenin transgenic thymocytes, respectively.
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Project description:CD5 is characterized as an inhibitory co-receptor with important regulatory role during T cell development. To study the molecular mechanism by which CD5 operates, we used quantitative mass spectrometry to analyze the components of the CD5 signaling machinery in primary T cells. In a first set of experiments, CD5-containing complexes were immunoprecipitated from thymocytes of wild-type (WT) C57BL/6 mice. Thymocytes were treated with pervanadate to induce widespread activation of protein tyrosine kinases. Corresponding samples prepared from thymocytes of Cd5−/− mice were used as controls, to discriminate CD5-binding molecules from the background of contaminant proteins. Eight biological replicates were prepared for both conditions, and samples were analyzed in duplicate LC-MS runs. This first set of experiment is presented in TableS1 of the paper, and is associated to the MaxQuant result file “Interactome WT” in the present PX dataset. We analyzed the CD5 interactome at different time of stimulation with pervanadate (1min and 10min) using thymocytes from wild-type (WT) C57BL/6 mice. Corresponding samples prepared from thymocytes of Cd5−/− mice were used as controls. Three biological replicates were prepared for both conditions (WT and KO) and each time point (1min and 10min). This set of experiments is presented in TableS2 of the paper and is associated to the MaxQuant result file “Interactome at 1min and 10min” in the present PX dataset. We checked that the activation of CD5 (phosphorylation sites) and the formation of the signaling complex was comparable in different stimulatory conditions (comparison of WT thymocytes stimulated with either pervanadate or anti-CD3+anti-CD4 antibodies). We also analyzed the binding of CD5 interactors in thymocytes from a c-Cbl-/- mouse model (comparison of WT and c-Cbl-/-thymocytes stimulated with pervanadate). These experiments and the associated experimental design of the comparisons are summarized in TableS3 of the paper, and are based on the MaxQuant result file “Comparison of different stimulatory conditions” in this dataset. To check the phosphorylation status of the CD5 tyrosine residues at different time of stimulation, we analyzed samples immunoprecipitated from thymocytes of wild-type (WT) C57BL/6 mice, following stimulation with anti-CD3+anti-CD4 antibodies for 1min, 3min and 10min. This set of experiment is presented in TableS4 of the paper and is associated to the MaxQuant result file “CD5 pY kinetics” in the present PX dataset. To determine the role of Y429 in the context of CD5 signaling, we expressed a wild-type (CD5tgWt) or a mutated form of CD5, containing a tyrosine to phenylalanine substitution at position 429 (CD5tgY429F) in transgenic mice. We analyzed the CD5 interactome by comparing samples immunoprecipitated from thymocytes of these 2 mice models (following pervanadate stimulation, 6 and 5 biological replicates respectively) with samples prepared in the same way from Cd5−/− mice as controls (6 biological replicates). The results are shown in TableS5 of the paper, and correspond to the MaxQuant result file “interactome CD5tgWt_CD5tgY429F”.
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Project description:TCF-1 is an HMG family transcription factor which is known to be critical for T cell development. We discovered that it has a unique role in suppressing malignant transformation of developing thymocytes at early stages. We identified ID2 and LEF-1 as key TCF-1 target genens in tumor suppression. We used microarrays to detect gene expression changes in WT and TCF-1 deficient DN3 thymocytes as well as T cell lymphoma cells developed in TCF-1 KO mice.
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Project description:TCF-1 is an HMG family transcription factor which is known to be critical for T cell development. We discovered that it has a unique role in suppressing malignant transformation of developing thymocytes at early stages. We identified ID2 and LEF-1 as key TCF-1 target genens in tumor suppression. We used microarrays to detect gene expression changes in WT and TCF-1 deficient DN3 thymocytes as well as T cell lymphoma cells developed in TCF-1 KO mice. DN3 thymocytes were directly sorted from WT or TCF-1 KO mice. T cell lymphoma blast cells were also sorted from TCF-1 KO mice that developed the disease. RNA was extracted and hybridized to GeneChip Mouse GENE 1.0 ST arrays (Affymetrix).
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