ChIP-chip from the follicular lymphoma cell line RL with H3K4me3, H3K37me3 and Suz12
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Huidong Shi
PROVIDER: E-GEOD-20019 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Maintenance of chromatin structure is essential to eukaryotic life; dysregulation is known to be causal for aberrant development and disease. The Mi-2/nucleosome remodeling and histone deacetylase (NuRD) complex is a multiprotein machine proposed to regulate chromatin structure by nucleosome remodeling and histone deacetylation activities. We identified the localization of MBD3, a component of Mi-2/NuRD complex, in two breast cancer cell lines (MCF7 and MDA-MB-231) using ChIP-Seq. MBD3 showed cell-type specific localization with overlap across cell lines being less than 50%. MBD3 localized across gene bodies, peaking around the transcription start site (TSS). Contrary to existing models, MBD3 preferentially associated with CpG rich promoters marked by H3K4me3. These data suggest that MBD3, and by extension the Mi-2/NuRD complex, may have roles in fine tuning expression for active genes. These data represent an important first step in defining regulatory mechanisms by which Mi-2/NuRD complex controls chromatin structure and gene expression. Identification of MBD3 localization in human breast cancer cell lines
2013-10-31 | E-GEOD-44737 | biostudies-arrayexpress
Project description:We conducted genome-wide bisulfite sequencing analysis of the follicular lymphoma cell line RL and found that a large amount of methylated genes are polycomb target genes in ES cells. We therefore conducted a ChIP-chip experiment to determine the methylated genes that are bound by the polycomb protein Suz12. Although 28% of MRIs are PRC2 target genes in ES cells, our ChIP-on-Chip analysis showed that only 13% of MRIs are associated with H3K27Me3 marks and only 5% of the MRIs are bound by Suz12 in RL cells in vivo.
2010-01-24 | GSE20019 | GEO
Project description:Cellular differentiation entails reprogramming of the transcriptome from a pluripotent to a unipotent fate. This process was suggested to coincide with a global increase of repressive heterochromatin, which results in a reduction of transcriptional plasticity and potential. Here we report the dynamics of the transcriptome and an abundant heterochromatic histone modification, dimethylation of histone H3 at lysine 9 (H3K9me2), during neuronal differentiation of embryonic stem cells. In contrast to the prevailing model, we find H3K9me2 to occupy over 50% of chromosomal regions already in stem cells. Marked are most genomic regions that are devoid of transcription and a subgroup of histone modifications. Importantly, no global increase occurs during differentiation, but discrete local changes of H3K9me2 particularly at genic regions can be detected. Mirroring the cell fate change many genes show altered expression upon differentiation. Quantitative sequencing of transcripts reveals however that the total number of active genes is equal between stem cells and several tested differentiated cell types. Together, these findings reveal high prevalence of a heterochromatic mark in stem cells and challenge the model of low abundance of epigenetic repression and resulting global transcription in stem cells. Instead cellular differentiation entails local rather than global changes in epigenetic repression and transcriptional activity. Our dataset comprises of 2 ChIP-seq samples using chromatin from embryonic stem (ES) cells and derived terminal neurons (TN) which was immunoprecipitated, using antibodies against H3K27me3 and H3K4me2. For the same cells we generated H3K9me2 ChIP-chip samples in biological replicates. For ES cells, neurons and mouse embryonic fibroblasts (MEFs) we generated biological replicates of RNA-seq data.
2011-06-21 | E-GEOD-27827 | biostudies-arrayexpress
Project description:To identify the MYCN transcription factor binding sites across the genome, we performed chromatin immunoprecipitation followed by sequencing (ChIP-seq) using anti-MYCN and anti-IgG antibodies on a MYCN-amplified NB cell line, SK-N-BE(2)-C. Identification of MYCN binding in neuroblastoma cells.
2016-05-16 | E-GEOD-72640 | biostudies-arrayexpress
Project description:To further study the transcriptome of THP-1 human monocytes after exposure to S-Nitrosoglutathione (GSNO), we investigate whole genome microarray expression to identify genes regulated by exposure or not to GSNO. To further study the transcriptome of THP-1 human monocytes after exposure for 4 h to 50 ug / mL of S-Nitrosoglutathione-loaded polymeric Eudragit RL nanoparticles (GSNO-loaded ENP), we investigate whole genome microarray expression to identify genes regulated by exposure or not to 50 ug / mL of GSNO-loaded ENP. To further study the transcriptome of THP-1 human monocytes after exposure for 4 h to 200 ug / mL of empty polymeric Eudragit RL nanoparticles (empty ENP), we investigate whole genome microarray expression to identify genes regulated by exposure or not to 200 ug / mL of empty ENP. To further study the transcriptome of THP-1 human monocytes after exposure for 24 h to 50 ug / mL of S-Nitrosoglutathione-loaded polymeric Eudragit RL nanoparticles (GSNO-loaded ENP), we investigate whole genome microarray expression to identify genes regulated by exposure or not to 50 ug / mL of GSNO-loaded ENP. To further study the transcriptome of THP-1 human monocytes after exposure for 24 h to 50 ug / mL of empty polymeric Eudragit RL nanoparticles (empty ENP), we investigate whole genome microarray expression to identify genes regulated by exposure or not to 50 ug / mL of empty ENP. To further study the transcriptome of THP-1 human monocytes after exposure for 4 h to 50 ug / mL of empty polymeric Eudragit RL nanoparticles (empty ENP), we investigate whole genome microarray expression to identify genes regulated by exposure or not to 50 ug / mL of empty ENP. To further study the transcriptome of THP-1 human monocytes after exposure for 4 h to 200 ug / mL of S-Nitrosoglutathione-loaded polymeric Eudragit RL nanoparticles (GSNO-loaded ENP), we investigate whole genome microarray expression to identify genes regulated by exposure or not to 200 ug / mL of GSNO-loaded ENP. Changes in gene expression in THP-1 cells incubated without (control) or with 50 uM GSNO for 4 h, were measured. Five biological replicates were performed as controls: F_01; F_07; F_13; S_01; S_02. Four biological replicates were performed in GSNO exposed cells: S_13; S_14; S_15; S_16. Changes in gene expression in THP-1 cells incubated without (control) or with 50 ug / mL of GSNO-loaded ENPs (300 nm) for 4 h were measured. Five biological replicates were performed as controls: F_01; F_07; F_13; S_01; S_02. Three biological replicates were performed in 50 ug / mL of GSNO-loaded ENP exposed cells: S_06; S_07; S_08. Changes in gene expression in THP-1 cells incubated without (control) or with 200 ug / mL of empty ENPs (300 nm) for 4 h were measured. Five biological replicates were performed as controls: F_01; F_07; F_13; S_01; S_02. Three biological replicates were performed in 200 ug / mL of empty ENP exposed cells: S_17; S_19; S_20. Changes in gene expression in THP-1 cells incubated without (control) or with 50 ug / mL of GSNO-loaded ENPs (300 nm) for 24 h were measured. Five biological replicates were performed as controls: F_04; F_10; F_16; S_03; S_04. Four biological replicates were performed in 50 ug / mL of GSNO-loaded ENP exposed cells: S_09; S_10; S_11; S_12. Changes in gene expression in THP-1 cells incubated without (control) or with 50 ug / mL of empty ENPs (300 nm) for 24 h were measured. Five biological replicates were performed as controls: F_04; F_10; F_16; S_03; S_04. Three biological replicates were performed in 50 ug / mL of empty ENP exposed cells: F_05; F_11; F_17. Changes in gene expression in THP-1 cells incubated without (control) or with 50 ug / mL of empty ENPs (300 nm) for 4 h were measured. Five biological replicates were performed as controls: F_01; F_07; F_13; S_01; S_02. Three biological replicates were performed in 50 ug / mL of empty ENP exposed cells: F_02; F_08; F_14. Changes in gene expression in THP-1 cells incubated without (control) or with 200 ug / mL of GSNO-loaded ENPs (300 nm) for 4 h were measured. Five biological replicates were performed as controls: F_01; F_07; F_13; S_01; S_02. Four biological replicates were performed in 200 ug / mL of GSNO-loaded ENP exposed cells: S_21; S_22; S_23; S_24.
2013-12-19 | E-GEOD-51186 | biostudies-arrayexpress
Project description:Although short-term disuse does not result in measurable muscle atrophy, studies suggest that molecular changes associated with protein degradation may be initiated within days of the onset of a disuse stimulus. We examined the global gene expression patterns in sedentary men (n = 7, mean age ± S.D = 22.1 ± 3.7 yr) following 48h unloading (UL) via unilateral lower limb suspension and 24h reloading (RL). Biopsy samples of the left vastus lateralis muscle were collected at baseline, 48h UL, and 24h RL. Expression changes were measured by microarray and gene clustering; identification of enriched functions and canonical pathways were performed using the Database for Annotation, Visualization and Integrated Discovery (DAVID) and Ingenuity Pathway Analysis (IPA). Four genes were validated with qRT-PCR, and protein levels were measured with Western blot. Of the upregulated genes after UL, the most enriched functional group and highest ranked canonical pathway were related to protein ubiquitination. The oxidative stress response pathway was the second highest ranked canonical pathway. Of the downregulated genes, functions related to mitochondrial metabolism were the mostly highly enriched. In general, gene expression patterns following UL persisted following RL. qRT-PCR confirmed increases in mRNA for UPP-related E3 ligase Atrogin1 (but not accompanying increases in protein products) and stress response gene heme oxygenase-1 (HMOX, which showed a trend towards increases in protein products at 48h UL) as well as extracellular matrix (ECM) component COL4. The gene expression patterns were not readily reversed upon RL suggesting that molecular responses to short-term periods of skeletal muscle inactivity may persist after activity resumes. Biopsies were taken of the left vastus lateralis of healthy, sedentary men (N = 7) at baseline, immediately following 48h UL and 24h RL. A 5mm Berstrom biopsy needle was used. Biopsy samples were immediately snap-frozen in liquid nitrogen upon excision. All samples were stored at -80° C until analysis.
2010-10-23 | E-GEOD-21496 | biostudies-arrayexpress
Project description:The H3K27me3 ChIP-seq data for the human bladder transitional cell carcinoma cell line CL1207 were generated in order to detect regions of regional epigenetic silencing in this cell line and test the performance of several peak calling tools: CCAT (Xu et al., 2010) and HMCan (Ashoor et al., "HMCan M-bM-^@M-^S a tool to detect chromatin modifications in cancer samples using ChIP-seq data", submitted). The human bladder cancer cell line CL1207 was derived from a muscle-invasive bladder cancer (De Boer et al., 1997). 5x105 cells were immunoprecipitated per ChIP assay with 4 M-NM-<g of rabbit polyclonal antibodies against trimethyl histone H3 lysine 27 (Upstate Biotechnology, Santa Cruz, CA) and DynabeadsM-BM-. Protein A (Invitrogen, Cergy Pontoise, France) in dilution buffer containing 1% Triton X-100, 150 mM NaCl, 2 mM EDTA, 20 mM TrisM-bM-^@M-^SHCl at pH 8.0, and protease inhibitors. Six ChIP assays in the same experimental conditions were necessary to perform one ChIP-Seq experiment, so the total of 3x106 cells for each of the duplicates.
2014-01-07 | E-GEOD-44438 | biostudies-arrayexpress
Project description:In this work, we generated hundreds of millions of Hi-C paired end sequence reads for three different human cells (RL follicular lymphoma cell line, primary tumor B-cells from an acute lymphoblastic leukemia patient, and MHH-CALL-4 B-cell acute lymphoblastic leukemia cell line) using the Hi-C technique. An in-house Bioinformatics software pipeline was developed and applied to map sequence reads to the human reference genome, producing a large data set of high-quality and high-resolution chromosome contacts. Our computational analysis on these data reveal some interesting properties of human genome conformation, including conformational conservation and variation of the genomes of different cells, intra- and inter-chromosomal interactions, aberrant chromosomal translocation, spatial gene clusters, spatial gene-gene interactions, and spatial gene-regulatory-element interaction. Furthermore, we derived spatial interactions between functional elements (genes, transcription factor binding sites) from the chromosomal interaction data. The data were then used to generate chromosome-/genome-wide gene-gene interaction networks, transcription factor binding site (TFBS) â TFBS networks, and gene-TFBS networks. Remarkably, the connectivity in both networks shows the hallmark features of scale-free networks, suggesting that spatial interactions of gene-gene, gene-TFBS, and TFBS-TFBS in a genome are far from random. Three different human cells (RL follicular lymphoma cell line, primary tumor B-cells from an acute lymphoblastic leukemia patient, and MHH-CALL-4 B-cell acute lymphoblastic leukemia cell line) were analyzed
2015-11-01 | E-GEOD-73924 | biostudies-arrayexpress
Project description:ChIP-chip from the follicular lymphoma cell line RL with H3K4me3, H3K37me3 and Suz12
| PRJNA124095 | ENA
Project description:Oct4 stemness gene encoding a transcription factor has been shown to overexpress in cancers. However, precise mechanisms of Oct4 relevant to transcriptional reprogramming leading to somatic cancer progression remain unclear. To address the Oct4-mediated transcriptional program in lung cancer, we integrated genome-wide Oct4 binding profiles from chromatin-immunoprecipitation sequencing and ENCODE datasets. We identified that Oct4 occupied at functional promoter and enhancer regions of genes which play key roles in several signaling pathways involving tumorigenesis. Genome-wide Oct4 binding sites were identified via chromatin immunoprecipitation-sequencing analysis of vecoter control and stably Oct4-overexpressing A549 lung cancer cells. ChIP-seq analyses were performed in duplicated samples using Applied Biosystems SOLiD system.
2015-02-04 | E-GEOD-58462 | biostudies-arrayexpress