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SRP068833
Mus musculus
4 Downloadable Samples
Ion Torrent Proton
Description
The goal of this study was to elucidate the effects of inflammation on bone metabolism. As we found IL-17A is induced immediately after bone injury and Il17a-/- mice showed delayed healing, we analyzed the effects of IL-17A on mesenchymal cells in the repair tissue. Most of the IL-17RA+ cells were PaS cells. We collected these cells and analyzed their response to IL-17A by RNA sequencing. This analysis will provide a mechanistic insight into the mechanism of how IL-17A promote bone formation in the context of bone fracture healing. Overall design: PaS cells were harvested from the injury tissue of wild-type mice and cultured with or without IL-17A or BMP-2. RNAs were harvested at day 7.
Publication Title
IL-17-producing γδ T cells enhance bone regeneration.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 10 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Fezf2 is highly and specifically expressed in mTECs in mouse thymus and Fezf2 deficiency (Fezf2 KO) in the thymus leads to autoimmunity. However, it is unclear how Fezf2 contributes to thymic gene expression.
Publication Title
Fezf2 Orchestrates a Thymic Program of Self-Antigen Expression for Immune Tolerance.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Screening for mouse cDNA that was highly expressed in positive-selector H-2b AND-TCR-transgenic thymocytes using Affymetrix Murine Genome arrays.
Publication Title
IAN family critically regulates survival and development of T lymphocytes.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
- Ion Torrent Proton
Description
Protein arginine methylation is a post-translational modification catalyzed by protein arginine methyltransferase (PRMT). To elucidate the role of PRMT5 in T cells, we generated T-cell specific PRMT5-deficient mice (Prmt5 flox/d Cd4-Cre mice) and found a severe loss of thymic iNKT cells as well as a reduced number in peripheral CD4+ and CD8+ T cells. As iNKT cells were significantly decreased in the stage 1, 2 and 3 of developmental stages, RNA-seq was performed using stage 1 iNKT cells of control and PRMT5-deficient mice. This transcriptome analysis will provide mechanistic insight into how PRMT5 contributes to thymic iNKT cell development. Overall design: Stage 1 iNKT cells were sorted from thymus of control and Prmt5 flox/D Cd4-Cre mice. Total RNA was extracted and RNA-seq was performed by Ion Proton.
Publication Title
Arginine methylation controls the strength of γc-family cytokine signaling in T cell maintenance.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 4 Downloadable Samples
- Illumina HiSeq 2500
Description
The pluripotent mammalian epiblast undergoes unusually fast cell proliferation. This rapid growth is expected to generate a high transcriptional demand, but the underlying mechanisms remain unknown. We report that the chromatin remodeler Chd1, which binds the activating histone mark H3K4me3 and is associated with transcription, is required for development of the mouse epiblast. Chd1-/- embryos exhibit proliferation defects and increased apoptosis, are smaller than controls by E5.5, and fail to grow, become patterned or gastrulate. We show that Chd1-/- ES cells have a self-renewal defect and a genome-wide reduction in transcriptional output that is associated with losses in RNA Pol II elongation at growth-promoting genes, including ribosomal proteins. We also report that Chd1 directly regulates ribosomal RNA transcription and that both Chd1-/- epiblast cells in vivo and ES cells in vitro express significantly lower levels of ribosomal RNA. Single cell analyses reveal abnormal nucleolar morphology in mutants in vivo and in vitro. These data indicate that Chd1 promotes a globally elevated transcriptional output required to sustain the distinct rapid growth of the mouse epiblast. Overall design: Cell-number normalized RNA-seq from wild-type and Chd1-/- mouse embryonic stem cells.
Publication Title
Chd1 is essential for the high transcriptional output and rapid growth of the mouse epiblast.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Evi1 is essential for proliferation of hematopoietic stem cells and implicated in the development of myeloid disorders. Particularly, high Evi1 expression defines one of the largest clusters in acute myeloid leukemia and is significantly associated with extremely poor prognosis. Improvement of the therapeutic outcome of leukemia with activated Evi1 is one of the most challenging issues. However, mechanistic basis of Evi1-mediated leukemogenesis has not been fully elucidated. Here we show that Evi1 directly represses PTEN transcription in the murine bone marrow, which leads to activation of AKT/mTOR signaling. In a murine bone marrow transplantation model, Evi1 leukemia showed remarkable sensitivity to an mTOR inihibitor rapamycin. Furthermore, we found that Evi1 binds to several polycomb group proteins and recruits polycomb repressive complexes for PTEN downregulation, which reveals a novel epigenetic mechanism of AKT/mTOR activation in leukemia. Expression analyses and chromatin immunoprecipitation assays using human samples indicate that our findings in mice models are recapitulated in human leukemic cells. Dependence of Evi1-expressing leukemic cells on AKT/mTOR signaling provides the first example of targeted therapeutic modalities that suppress the leukemogenic activity of Evi1. The PTEN/AKT/mTOR signaling pathway and the Evi1-polycomb interaction can be promising therapeutic targets for leukemia with activated Evi1.
Publication Title
Evi1 represses PTEN expression and activates PI3K/AKT/mTOR via interactions with polycomb proteins.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Rattus norvegicus
- 6 Downloadable Samples
- Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
In order to define the transcriptional network functionally regulated by Pax8 as well as infer its direct targets, we performed RNAi to knock-down Pax8 gene in FRTL-5 thyroid cells. Expression data from three independent silencing experiments were analyzed by microarray technology unraveling 2815 genes differentially expressed between silenced cells and controls. Of these, 1421 genes were down-regulated and 1394 genes were up-regulated 72hrs after Pax8 silencing.
Publication Title
Identification of novel Pax8 targets in FRTL-5 thyroid cells by gene silencing and expression microarray analysis.
Sample Metadata Fields
Cell line
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
- 10 Downloadable Samples
- Affymetrix HT Human Genome U133A Array (hthgu133a)
Description
U87MG is a glioblastoma cell line that shows substantial heterogeneity despite long-term passaging.
Publication Title
Dynamic epigenetic regulation of glioblastoma tumorigenicity through LSD1 modulation of MYC expression.
Sample Metadata Fields
Cell line
View Samples- Arabidopsis thaliana
- 12 Downloadable Samples
- Arabidopsis Gene 1.0 ST Array (aragene10st)
Description
The AIL transcription factor BABY BOOM (BBM) is required together with the related PLETHORA proteins for embryo and root meristem development and its expression is sufficient to confer pluripotency and totipotency to somatic tissues. We show that BBM and other AIL proteins interact with multiple members of the L1/epidermal-expressed HD-ZIP class IV / HOMEODOMAIN GLABROUS (HDG) transcription factor family. Ectopic overexpression of HDG1, HDG11 and HDG12 genes induces a reduced growth phenotype, and analysis of HDG1 overexpression lines shows that this growth reduction is due to both root and shoot meristem arrest. To understand how HDG1 controls cell proliferation, as well as its functional relationship with BBM, we performed microarray experiments to identify candidate genes that are directly regulated by HDG1, and compared these to the set of genes that are directly regulated by BBM expression.
Publication Title
AIL and HDG proteins act antagonistically to control cell proliferation.
Sample Metadata Fields
Specimen part, Treatment
View Samples