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ChIPseq of PPARbeta/delta in MDA-MB-231luc cells

ABSTRACT: Chromatin-immunoprecipitated with antiPPARD and antiRXR antibodies was performed in MDA-MB-231luc1 cells.

ORGANISM(S): Homo_sapiens

DISEASE(S): breast carcinoma

SUBMITTER: Florian Finkernagel

PROVIDER: E-MTAB-1097 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Inverse PPARβ/δ agonists suppress oncogenic signaling to the ANGPTL4 gene and inhibit cancer cell invasion.

Adhikary T T Brandt D T DT Kaddatz K K Stockert J J Naruhn S S Meissner W W Finkernagel F F Obert J J Lieber S S Scharfe M M Jarek M M Toth P M PM Scheer F F Diederich W E WE Reinartz S S Grosse R R Müller-Brüsselbach S S Müller R R

Oncogene 20121203 44

Besides its established functions in intermediary metabolism and developmental processes, the nuclear receptor peroxisome proliferator-activated receptor β/δ (PPARβ/δ) has a less defined role in tumorigenesis. In the present study, we have identified a function for PPARβ/δ in cancer cell invasion. We show that two structurally divergent inhibitory ligands for PPARβ/δ, the inverse agonists ST247 and DG172, strongly inhibit the serum- and transforming growth factor β (TGFβ)-induced invasion of MDA ...[more]

PMID: 23208498

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Genome-wide analyses define different classes of PPARbetadelta target genes characterized by distinct modes of transcriptional regulation (Sequencing)

Project description:Genome-wide occupancy of PPARbeta/delta in human myofibroblast (WPMY-1 celline) was studied with ChIP-Seq. Additionally, H3K4 trimethylation and RNA polymerase II status was examined.

2010-12-31 | E-MTAB-371 | biostudies-arrayexpress

Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers [ChIP-seq]

Project description:Scl/Tal1 confers hemogenic competence and prevents cardiomyogenesis in embryonic endothelium. Here we show that Scl both directly activates a broad gene regulatory network required for hematopoietic stem/progenitor cell (HS/PC) development, and represses transcriptional regulators required for cardiogenesis. Cardiac repression occurs during a short developmental window through Scl binding to distant cardiac enhancers that harbor H3K4me1 at this stage. Scl binding to hematopoietic regulators extends throughout HS/PC and erythroid development and spreads from distant enhancers to promoters. Surprisingly, Scl complex partners Gata 1 and 2 are dispensable for hematopoietic versus cardiac specification and Scl binding to the majority of its target genes. Nevertheless, Gata factors co-operate with Scl to activate selected transcription factors to facilitate HS/PC emergence from hemogenic endothelium. These results uncover a dual function for Scl in dictating hematopoietic versus cardiac fate choice and suggest a mechanism by which lineage-specific bHLH factors direct the divergence of competing fates. ChIP-seq with Scl, Hand1, Lsd1, Ezh2, H3K4me1 and H3K27ac in different cell types with mesodermal origin. Scl ChIP-seq in WT, SclKO, SclKO-iScl and Gata12KO mES cell derived day4 EB (embryoid body) Flk1+ mesodermal cells, SclKO-iScl ES cells and MEL cells; Hand1 ChIP-seq in WT mES cell derived day4 EB Flk1+ mesodermal cells; Lsd1 and Ezh2 ChIP-seq in WT and SclKO mES cell derived day4 EB Flk1+ mesodermal cells. ChIP-seq of histone modifications H3K4me1 and H3K27ac in WT, SclKO and Gata12KO mES cell derived day4 EB Flk1+ mesodermal cells, HPC7 hematopoietic progenitor cells and HL1 cardiomyogenic cells

2015-01-01 | E-GEOD-47082 | biostudies-arrayexpress

Physiological Vascular Permeability Requires Induction of Endothelial NR4A1 by Progesterone Receptor [ChIP-Seq]

Project description:Vascular permeability is frequently associated with inflammation and it is triggered by chemokines and by a cohort of secreted permeability factors, such as VEGF. In contrast, here we showed that the physiological vascular permeability that precedes implantation is directly controlled by progesterone receptor (PR) and it is independent of VEGF. Both global and endothelial-specific deletion of PR block physiological vascular permeability in the uterus while misexpression of PR in the endothelium of other organs results in ectopic vascular leakage. Integration of genome-wide transcriptional profile of endothelium and ChIP-sequencing revealed that PR induces a NR4A1 (Nur77/TR3) specific transcriptional program that broadly regulates vascular permeability in response to progesterone. This program triggers concurrent suppression of several junctional proteins and leads to an effective, timely and venule-specific regulation of vascular barrier function. Silencing NR4A1 blocks PR-mediated permeability responses indicating a direct link between PR and NR4A1. These results reveal a previously unknown function for progesterone receptor on endothelial cell biology with consequences to physiological vascular permeability and implications to the clinical use of progestins and anti-progestins on blood vessel integrity. Examination of PR binding sites in HUVEC cells using ChIP-seq (non-infected-negative control, PR infected followed by ligand treatment-PR+P or vehicle PR)

2014-01-01 | E-GEOD-43786 | biostudies-arrayexpress

ChIP-seq data of Epstein-Barr Virus Nuclear Antigen Leader ProteinM-BM- (EBNALP)

Project description:Epstein-Barr-Virus (EBV) Nuclear Antigens EBNALP and EBNA2 are co-expressed in EBV infected B-lymphocytes and are critical for Lymphoblastoid Cell Line (LCL) growth. EBNALP removes NCOR1 and RBPJ repressive complexes from promoter and enhancer sites and EBNA2 mostly activates transcription from distal enhancers. ChIP-seqs found EBNALP at 19,224 LCL sites, which were 33% promoter associated. EBNALP was associated with 10 transcription factor (TF) clusters that included YY1(63%), SP1(62%), PAX5(59%), BATF(50%), IRF4(49%), RBPJ(43%), ETS1(39%), PU.1(37%), RAD21(33%), NF-kB(31%), TBLR1(26%), ZNF143(24%), CTCF(23%), SMC3(21%), and EBF(17%). EBNALP sites had higher H3K4me3, H3K9ac, H3K27ac, H2Az, and RNA Pol II signals than EBNA2 sites and had similar transcription effects. EBNALP co-localized with 29% of 19,845 EBNA2 sites. EBNALP/EBNA2 sites were similar to EBNALP sites in promoter localization, associated cell TFs, Pol II, H3K4me3, H3K9ac, H3K27ac, and H2Az signals. EBNALP and EBNA2 promoter sites were more transcriptionally active than EBNALP or EBNA2 promoter sites. EBNALP was at the enhancer or promoter of myc and MYC affected genes, including cyclin D2, and bcl2. EBNALP at promoters with DNA looping and transcription factors, is positioned to deplete repressors from enhancers and promoters, enable chromatin remodeling, and transcription activation. Two EBNALP ChIP-seq replicates from IB4 LCL are analyzed in this study.

2013-07-31 | E-GEOD-49338 | biostudies-arrayexpress

MLL and Pol2 Chip-chip in interphase and mitotic arrested cells

Project description:Mixed Lineage Leukemia (MLL) and its metazoan Trithorax orthologs have been linked with the epigenetic maintenance of transcriptional activity. To identify mechanisms by which MLL perpetuates active transcription in dividing cells, we investigated its role during M-phase of the cell cycle. Unlike other chromatin modifying enzymes examined, we found that MLL associates with gene promoters packaged within condensed mitotic chromosomes. Genome-wide location analysis identified a globally rearranged pattern of MLL occupancy during mitosis in a manner favoring genes that were highly transcribed during interphase. Knockdown experiments revealed that MLL retention at gene promoters during mitosis accelerates transcription reactivation following mitotic exit. MLL tethers Menin, RbBP5, and ASH2L to its occupied sites during mitosis, but is dispensable for preserving histone H3K4 methylation. These findings implicate mitotic bookmarking as a component of Trithorax-based gene regulation which may facilitate inheritance of active gene expression states during cell division. anti-MLL ChIP (antibody 456) and anti-pol2 chip (sc-899) in chromatin prepared from interphase and mitotic HeLa cells

2010-05-19 | E-GEOD-19155 | biostudies-arrayexpress

Activation of the Integrated Stress Response by a Jumonji Histone Demethylase Inhibitor Induces Pro-Apoptotic Metabolic Reprogramming in Multiple Myeloma

Project description:Regulation of gene expression by chromatin modification through methylation of histone lysine residues is a dynamic, reversible process that when deregulated is associated with cancer development. In multiple myeloma, combined inhibition of the histone demethylases JARID1B, UTX and JmjD3 by the small molecule GSK-J4 prevents cellular glutamine utilization leading to amino acids deprivation, activates the integrated stress response via GCN2-dependent ATF4 activation, and induces apoptosis. This response is associated with a profound upregulation of metallothionein genes. Combined with clinical data demonstrating that overexpression of JARID1B is associated with shorter survival in multiple myeloma patients, this study highlights histone demethylases as epigenetic drug targets and places this demethylase inhibitor chemotype as having unique potential relative to established anti-myeloma treatment options. In total there are 7 different samples analyzed and one input control. Treatments are carried out with the demethylase inhibitor (or DMSO as negative control) at 6h and 48h, or with LNA targeting demethylases (or scrambled LNA) at 7 days. A negative control at 0h is included.

2015-08-21 | E-GEOD-60626 | biostudies-arrayexpress

Macro histone variants preserve cell identity by preventing the gain of H3K4me2 during reprogramming

Project description:Transcription factor-induced reprogramming of somatic cells to pluripotency is a very inefficient process, probably due to the existence of important epigenetic barriers that are imposed during differentiation and that contribute to preserve cell identity. In an effort to decipher the molecular nature of these barriers, we followed a genome-wide approach, in which we identified macro histone variants (macroH2A) as highly expressed in human somatic cells but downregulated after reprogramming to pluripotency, as well as strongly induced during differentiation. Knock down of macro histone variants in human keratinocytes increased the efficiency of reprogramming to pluripotency, while overexpression had opposite effects. Genome-wide occupancy profiles show that in human keratinocytes macroH2A.1 preferentially occupies genes that are expressed at low levels and are marked with H3K27me3, including pluripotency-related genes and bivalent developmental regulators, at which its presence prevents the regain of H3K4me2 during reprogramming, over imposing an additional layer of repression that preserves cell identity. Gemone wide occupancy of HA:macroH2A.1 in human keratinocytes

2013-04-03 | E-GEOD-44400 | biostudies-arrayexpress

MEIS1 ChIPseq in CHRF-288-11

Project description:ChIP-seq of MEIS1 in the human megakaryocytic cell line CHRF-288-11

2012-01-04 | E-MTAB-859 | biostudies-arrayexpress

CTCF/CP190 and ISWI dependent regulation of nucleosome occupancy [ChIP-seq]

Project description:H3-ChIP-seq was performed in order to analyze changes in nucleosomal occupancy after depletion of CTCF/P190 and ISWI from Drosophila S2 cells Histone H3 ChIP-seq from Drosophila S2 cells after CTCF/CP190 or ISWI-specific RNAi treatment

2014-08-11 | E-GEOD-51598 | biostudies-arrayexpress

ChIP-chip analysis of GBF1 in the presence and absence of its heterodimerizing partners, HY5 and HYH

Project description:Transcription factors are key components of light signalling as they amplify the signal, which results in massive changes in genome-wide expression during photomorphogenesis. Three bZIP transcription factors (TFs), namely GBF1, HY5, and HYH, form heterodimers with each other and regulate photomorphogenesis in an interdependent manner. GBF1 acts as both a positive and negative regulator of photomorphogenesis, whereas HY5 and HYH mainly act as positive regulators of photomorphogenesis. In this study, the impact of heterodimerization of GBF1 with HY5 and HYH was analyzed for genome-wide binding of GBF1 through ChIP-chip in GBF1. We identified more than 2000 direct targets of GBF1 in the presence of HY5 and HYH. However, in the absence of HY5, very few binding sites were found, and in the absence of functional HYH protein, the number of GBF1 direct targets reduced to only half compared to when functional HYH was present. ChIPed DNA with GBF1 antibody from GBF1OE, hy5 GBF1OE, and hyh GBF1OE lines vs. ChIPed DNA with GBF1 antibody from wild-type.

2014-03-24 | E-GEOD-36965 | biostudies-arrayexpress

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