Genome-wide profilings of IFN-stimulated murine splenic B cells by ATAC-Seq.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: CBDM Lab
PROVIDER: E-GEOD-75262 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:We report the IFN-induced dynamics in murine splenic B cells. Male C57BL/6 mice were injected subcutaneously with 10,000U IFNa and spleens were removed at designated time. B cells were negatively isolated using magnetic beads and profiled for the binding of PolII and Stat2 by ChIP-seq analysis. Profilings by PolII ChIP-seq over the time course (0, 0.5, 1, 2, 4, 8, 24 and 48hrs, single replicate for each), Stat2 ChIP-seq (0 and 90min, biological duplicate for each).
2015-11-21 | E-GEOD-75250 | biostudies-arrayexpress
Project description:We report the IFN-induced dynamics in murine splenic B cells. Male C57BL/6 mice were injected subcutaneously with 10,000U IFNa and spleens were removed at 90min. B cells were negatively isolated using magnetic beads and profiled for the chromatin configuration by ATAC-seq.
2015-11-21 | GSE75262 | GEO
Project description:We report the IFN-induced dynamics in murine splenic B cells. Male C57BL/6 mice were injected subcutaneously with 10,000U IFNa and spleens were removed at designated time. B cells were negatively isolated using magnetic beads and profiled for the binding of PolII and Stat2 by ChIP-seq analysis.
2015-11-21 | GSE75250 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2015-11-24 | E-GEOD-75306 | biostudies-arrayexpress
Project description:Purpose: To identify the molecular phenotype of endothelial cells (EC) isolated from the unique vasculature of the corpus cavernosum. Methods: Human EC derived from corpus cavernosum (HCCEC, n=5), coronary artery (HCAEC, n=4) and umbilical vein (HUVEC, n=3) were grown in culture and mRNA transcripts quantified by Affymetrix GeneChip microarrays. Genes differentially expressed across samples were partitioned around medoids to identify genes with highest expression in HCCEC. Several genes were verified by real-time PCR. The role of claudin 11 (CLDN11) in endothelial cell barrier function was examined by in vitro transendothelial electrical resistance assay. Results: Unsupervised hierarchical clustering of samples using all expressed genes yielded discrete groupings of EC lines according to their in vivo source of origin. 190 genes/transcripts were highly expressed only in cavernosal HCCEC. Gene Ontology classification indicated cavernosal enrichment in genes related to cell adhesion, extracellular matrix (ECM), pattern specification and organogenesis. KEGG pathway analysis showed high expression of gene relating to ECM-receptor interaction, focal adhesions, and cytokine-cytokine receptor interaction. Real-time PCR confirmed expression differences in cadherins 2 and 11, CLDN11, desmoplakin and versican. CLDN11, a component of tight junctions not previously described in ECs, was highly expressed only in HCCEC and its knockdown by siRNA significantly reduced transendothelial electrical resistance in HCCEC. Conclusions: HCCECs displayed expression of transcripts encoding matrix and adhesion proteins that regulate structural and functional characteristics of blood vessels. High expression of the tight junction protein CLDN11 is novel in endothelial cells and contributes to barrier function of cultured HCCEC. Experiment Overall Design: Endothelial cells were grown on 2% gelatin type B (Sigma)/15% fetal bovine serum (Gibco) coated tissue culture dishes in Medium 199 (Gibco) supplemented with 20% FBS, EGM-2MV (Clonetics), L-glutamine and 10,000u/ml Penicillin, 10,000u/ml Streptomycin, and 25mg/ml Fungizone. All cells were grown in a humidified incubator at 37 oC and 5% CO2 with media changed every 2-3 days. Total RNA isolation for the arrays was performed using Qiagen RNeasy mini columns according to manufacturers instructions (RNeasy Mini Handbook). Briefly, cells grown in T-75 culture flasks were trypsinized with 0.25% trypsin/1 mM EDTA (Gibco) between the third and seventh passages and centrifuged to pellet the cells. Next, cells were disrupted and homogenized in RNeasy lysis buffer using a 1ml syringe with 21-gauge needle. Ethanol was added to allow binding of RNA to the silica-gel-based membrane of the mini column. Several washes as well as on-column DNase treatment were used to ensure that contaminants and DNA were effectively removed from the column. Finally, RNA was eluted in approximately 30ul of RNase free water. Experiment Overall Design: Biotin labeled target cRNA was prepared according to the Affymetrix eukaryotic target labeling protocol starting with 5ug total RNA for each sample. Each target was hybridized to an Affymetrix Human U133A GeneChip. GeneChips were washed and scanned at the University of Washingtonâs Center for Expression Arrays according to procedures developed by the manufacturer.
2009-10-03 | E-GEOD-10804 | biostudies-arrayexpress
Project description:Nanog, a core pluripotency factor in the inner cell mass of blastocysts, is also expressed in unipotent primordial germ cells (PGC) in mice1, where its precise role is yet unclear2-4. We investigated this in an in vitro model, where naïve pluripotent embryonic stem cells (ESCs) cultured in bFGF/ActivinA develop as epiblast-like cells (EpiLCs), and gain competence for PGC-like fate5. Consequently, bone morphogenetic protein (BMP4), or ectopic expression of key germline transcription factors Prdm1/ Prdm14/ Tfap2c, directly induce PGC-like cells (PGCLCs) in EpiLCs, but not in ESCs6-8. Here we report an unexpected discovery that Nanog alone can induce PGCLCs in EpiLCs, independently of BMP4. We propose that following the dissolution of the naïve ESC pluripotency network during establishment of EpiLCs9,10, the epigenome is reset for cell fate determination. Indeed, we found genome-wide changes in NANOG binding pattern between ESCs and EpiLCs, indicating epigenetic resetting of regulatory elements. Accordingly, we show that NANOG can bind and activate enhancers of Prdm1 and Prdm14 in EpiLCs in vitro; BLIMP1 (encoded by Prdm1) then directly induces Tfap2c. Furthermore, while SOX2 and NANOG promote the pluripotent state in ESCs, they show contrasting roles in EpiLCs since Sox2 specifically represses PGCLC induction by Nanog. This study demonstrates a broadly applicable mechanistic principle for how cells acquire competence for cell fate determination, resulting in the context-dependent roles of key transcription factors during development. Nanog ChIP-seq
2016-01-11 | E-GEOD-71932 | biostudies-arrayexpress
Project description:To investigate how chromatin is shaped during inflammation geared towards the development of fibrosis in peritoneal tissue, we performed ATAC-seq in peritoneal membranes from wt and Il-6 knockout mice challenged with SES (a lyophilized cell-free supernatant prepared from Staphylococcus epidermidis ) together with Th1 polarised CD4+ T-cells administered via the intraperitoneal route. Peritoneal membrane was harvested 3 hours after injection, immediately snap-frozen in liquid nitrogen, and stored at -80C until processed. Tissues were diced and ground to a fine powder with intermittent addition of liquid nitrogen and Omni-ATAC-seq was performed.
2022-04-04 | E-MTAB-10739 | biostudies-arrayexpress
Project description:To identify the accessible chromatin in wild-type mouse embryonic stem cells (mESCs), we performed ATAC-seq in mESCs.
2021-01-05 | E-MTAB-9245 | biostudies-arrayexpress
Project description:To study the epigenetic regulation of intestinal epithelium we focus on the role of chromatin modulators. Lysine-specific histone demethylase 1a (KDM1A, LSD1) is one of the enzymes that can erase the H3K4me1/2 mark. To assess the role of LSD1 in intestinal epithelium we studied wild type (WT) (Villin-Cre -; Lsd1f/f) and intestinal-epithelial-specific knock-out (KO) (Villin-Cre+; Lsd1f/f) mice. We found that KO mice completely lack Paneth cells, and have altered stem cell characteristics compared to WT littermates. To assess genome-wide ATAC levels in WT and KO small intestines, we isolated intestinal epithelium tissue from wild type mice and LSD1 KO mice. This tissue was digested to single cells and performed ATAC seq as described in the protocols.
2021-03-23 | E-MTAB-8718 | biostudies-arrayexpress
Project description:Pharmacological intervention of redox balance in cancer cells often results in oxidative stress-mediated apoptosis, attracting much attention for the development of a new generation of targeted therapy in cancer. However, little is known about mechanisms underlying the conversion from oxidative signaling to downstream activities leading cells to death. We here report a systematic detection of transcriptome changes in response to oxidative signals generated in leukemia cells upon fenretinide treatment, implicating the occurrence of numerous stress-responsive events during the fenretinide induced apoptosis, such as redox response, endoplasmic reticulum stress/unfolded protein response, translational repression and proteasome activation. Moreover, the configuration of these relevant events is primarily orchestrated by stress responsive transcription factors, as typically highlighted by NF-E2-related factor-2 (NRF2) and heat shock factor 1 (HSF1). Several lines of evidence suggest that the coordinated regulation of these transcription factors and thus their downstream genes are involved in converting oxidative signaling into downstream stress-responsive events regulating pro-apoptotic and apoptotic activities at the temporal and spatial levels, typifying oxidative stress-mediated programmed death rather than survival in cancer cells. This study provides a roadmap for understanding oxidative stress-mediated apoptosis in cancer cells, which may be further developed into more sophisticated therapeutic protocols, as implicated by synergistic induction of cell apoptosis using proteasome inhibitors with fenretinide. Time-series experiment, fenretinide treated NB4 cells at 19 time points (i.e., 0.25, 0.5, 1, 2, 4, 6, 8, 10, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54 and 60 hours) and untreated NB4 cells at 4 time points (i.e., 0, 8, 12 and 15 hours).
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