Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA304470 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2966960_1.fastq.gz | Fastqsanger.gz | |||
| SRR2966960_2.fastq.gz | Fastqsanger.gz | |||
| SRR2966961_1.fastq.gz | Fastqsanger.gz | |||
| SRR2966961_2.fastq.gz | Fastqsanger.gz | |||
| SRR2966962_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 18 |
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Project description:Epigenetic profiling of mouse bone marrow derived mast cells (BMMCs) [ChIP-seq]
| PRJNA304469 | ENA
Project description:Gene expression profile of Pafah2-deficient bone marrow derived mast cells (BMMCs) treated with w3 epoxides or GW9662
2017-02-07 | GSE94527 | GEO
Project description:PEST-domain-enriched tyrosine phosphatase (PEP) is a cytoplasmic protein tyrosine phosphatase that regulates immune cell functions, including mast cell functions. Using bone marrow derived mast cells (BMMCs) from PEP+/+ and PEP-/- mice, RNA-seq data showed that dinitrophenol (DNP) - activated PEP-/- BMMCs have misregulated gene expression, with some cytokine/chemokine genes (eg.TNFα, IL13, CSF2) showing reduced gene expression in the dinitrophenol (DNP) - activated PEP-/- BMMCs compared to (DNP)-activated PEP+/+ BMMCs. Also, the ability of the glucocorticoid dexamethasone (Dex) to negatively regulate DNP - induced COX-2 gene expression in PEP-/- BMMCs was inhibited compared to the PEP+/+ BMMCs.
2018-01-31 | GSE108972 | GEO
Project description:Microenvironment-based alterations in mast cell phenotypes influence the susceptibility to anaphylaxis, yet the mechanisms underlying proper maturation of mast cells toward an anaphylaxis-sensitive phenotype are incompletely understood. Here we report that PLA2G3, a mammalian homolog of anaphylactic bee venom phospholipase A2, regulates this process. PLA2G3 secreted from mast cells is coupled with fibroblastic lipocalin-type PGD2 synthase (L-PGDS) to provide PGD2, which facilitates mast cell maturation via PGD2 receptor (DP1). Mice lacking PLA2G3, L-PGDS or DP1, mast cell-deficient mice reconstituted with PLA2G3- or DP1-null mast cells, or mast cells cocultured with L-PGDS-ablated fibroblasts exhibited impaired mast cell maturation and anaphylaxis. Thus, we describe a lipid-driven PLA2G3-L-PGDS-DP1 loop that drives mast cell maturation. Mast cell maturation; immature and mature bone marrow-derived mast cells (BMMCs); Four-condition experiment (mature BMMCs vs immature BMMCs, Pla2g3M-bM-^@M-^S/M-bM-^@M-^S vs Pla2g3+/+); 3 replicates of Pla2g3+/+ BMMCs, 4 replicates of Pla2g3M-bM-^@M-^S/M-bM-^@M-^S BMMCs, 4 replicates of Pla2g3+/+ cocultured BMMCs, 3 replicates of Pla2g3M-bM-^@M-^S/M-bM-^@M-^S cocultured BMMCs
2013-03-09 | E-GEOD-44980 | biostudies-arrayexpress
Project description:Purpose:The purpose of this study is to detect activated or silenced genes during Tet2-deficient bone marrow derived mast cell (BMMC) and the control cells. Gene expression differences between two samples could be found using transcriptome profiling (RNA-seq) analysis. Methods:Mouse BMMCs were generated from bone marrow cells in RPMI-1640 medium with recombinant mouse IL-3 and SCF. BMMCs were stained to confirm the surface expression of FcɛRI and c-Kit. Cells with purity >97.5% were used for subsequent experiments. BMMCs RNA profiles were generated by deep sequencing,using Illumina. Results: We mapped about 10 million sequence reads per sample to the mouse genome, identified hundreds of genes with significant mRNA variation between Tet2-deficient BMMC and the control cells.
2018-01-25 | GSE100560 | GEO
Project description:Mast cells are generally classified into two phenotypically distinct populations: mucosal-type mast cells (MMCs) and connective tissue-type mast cells (CTMCs). However, the molecular basis determining the different characteristics of the mast cell subclasses still remains unclear.Here, we report the characterization of MMCs and CTMCs derived from mouse bone marrow mast cells (BMMCs).
2022-07-28 | GSE135148 | GEO
Project description:The aim of this study was to investigate microRNA expression pattern and its functional relevance on the commitment toward mucosal differentiation and on IgE-mediated activation of mast cells. To identify microRNA genes the expression of which change during the differentiation and activation of murine primary mast cells in vitro, the putative committed progenitors (c-kit+ cells isolated on day 6 from differentiating cultures), immature mast cells (BMMC), mucosal-type mast cells (MMC), and IgE-activated mast cells were compared by Agilent microRNA array. RNA was isolated by miRNeasy (Qiagen) from: 1) c-kit+ cells, isolated from differentiating cultures (in the presence of IL3 and SCF) derived from the bone marrow using MACS column purification, 2) immature BMMCs obtained by cultivation of bone marrow cells in the presence of IL3 and SCF for 4 weeks, 3) mucosal-type mast cells by additional differentiation of immature BMMCs for 5 days by supplementation of IL9 and TGFbeta, and 4) activated mast cells by presensitization with anti-DNP IgE followed by IgE-crosslinking by DNP-antigen challenge for 2 hours. Agilent microRNA microarray was run on these experimental groups. Four biological replicates were included in every experimental group.
2011-01-01 | E-GEOD-24321 | biostudies-arrayexpress
Project description:Intestinal mucosal mast cells are critically involved in the development of food-induced allergic disorders. However, factors that induce differentiation of mucosal mast cells in the intestinal mucosa are largely unknown. To identify factors involved in mucosal mast cell differentiation, we compared the gene expression profiles between mucosal mast cells isolated from the small intestine and bone marrow-derived mast cells cultured in the presence of TGF-β or Notch ligand. Mucosal mast cells were isolated from the small intestine of naïve BALB/c mice by flow cytometry. Bone marrow-derived mast cells (BMMCs) were generated by culturing BALB/c bone marrow cells with murine interleukin-3 and stem cell factor for 3-4 weeks, and then cells were cultured for 6 days in the presence or absence of TGF-β or Delta-like 1 (Dll1), which is a Notch ligand. Total RNAs extracted from these cells were processed and hybridized to Affymetrix GeneChips.
2016-06-15 | E-GEOD-80139 | biostudies-arrayexpress
Project description:We found that AhR, a unique chemical sensor, is critical in controlling mast cell differentiation, growth and function in vitro and in vivo. This study seeks to further the understanding of the mechanisms of how AhR control mast cell homeostasis. Three different batches of bone marrow derived mast cells (BMMCs) from AhR null, AhR_d and normal control mice were cultured in 30% WEHI-3-conditioned medium. BMMCs were purified by negative selection with MicroBeads (Miltenyi Biotec) after 4 weeks in culture. 99% BMMCs were FcM-NM-5RI+ c-kit+ CD49b- by flow cytometry analysis. The cells were further rested in cytokine free medium for 4h. Subsequently, total RNA was collected. Gene expression profiling was performed on total RNA from mast cells using Illumina SentrixM-BM-. Murine Ref8_v2_R3 BeadChips. Details of the design and the gene signatures found are given in the paper associated with this GEO Series: Yufeng Zhou, Hui-Ying Tung, Ying-Ming Tsai, Shih-Chang Hsu, Hui-Wen Chang, Hirokazu Kawasaki, Hsiao-Chun Tseng, Beverly Plunkett, Peisong Gao, Chih-Hsin Hung, Becky M. Vonakis, and Shau-Ku Huang. M-bM-^@M-^\Aryl hydrocarbon receptor controls murine mast cell homeostasisM-bM-^@M-^], Blood 2013 Mar 5 [Epub ahead of print]
2013-04-01 | E-GEOD-44715 | biostudies-arrayexpress
Project description:Purpose: To transcriptome widely reveal 5-mC regulation by Tet2, we performed bisulfite-sequencing of mRNAs from Tet2-deficient BMMCs and the control cells.Methods: Mouse BMMCs were generated from bone marrow cells in RPMI-1640 medium with recombinant mouse IL-3 and SCF. BMMCs were stained to confirm the surface expression of FcɛRI and c-Kit. Cells with purity >97.5% were used for RNA isolation. Results: We carried out an unbiased global analysis of m5C in poly(A)RNA of mouse bone marrow derived mast cells (BMMCs).We show that there were indeed much more mCs in Tet2-deficient group compared with the control, more than half of which located in genic region. Furthermore, we observed that although much less mCs distributed in the three elements of exon regions, more mCs located in 3`-UTR for Tet2-deficient group compared with the control.
2018-01-25 | GSE100719 | GEO