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Co-activation of GR and NF-kB leads to extensive rearrangemnet of their binding sites and target genes

ABSTRACT: Global identification of activated GR and p65 binding sites and target genes using ChIP-seq in HeLa B2 cells. generation genome-wide chromatin state-maps of GR, p65 and RNAPII in HeLa B2 cells under conditions 1) DMSO (control); 2) TA 1M-BM-5M 4hr; 3) TNFM-NM-1 10ng/ml ; 4) TA 1M-BM-5M 4hr at at third hour 10ng/ml TNF M-NM-1 was added

ORGANISM(S): Homo sapiens

SUBMITTER: H.G. Stunnenberg

PROVIDER: E-GEOD-24518 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Coactivation of GR and NFKB alters the repertoire of their binding sites and target genes.

Rao Nagesha A S NA McCalman Melysia T MT Moulos Panagiotis P Francoijs Kees-Jan KJ Chatziioannou Aristotelis A Kolisis Fragiskos N FN Alexis Michael N MN Mitsiou Dimitra J DJ Stunnenberg Hendrik G HG

Genome research 20110712 9

Glucocorticoid receptor (GR) exerts anti-inflammatory action in part by antagonizing proinflammatory transcription factors such as the nuclear factor kappa-b (NFKB). Here, we assess the crosstalk of activated GR and RELA (p65, major NFKB component) by global identification of their binding sites and target genes. We show that coactivation of GR and p65 alters the repertoire of regulated genes and results in their association with novel sites in a mutually dependent manner. These novel sites pred ...[more]

PMID: 21750107

Similar Datasets

Co-activation of GR and NF-kB leads to extensive rearrangemnet of their binding sites and target genes

Project description:Global identification of activated GR and p65 binding sites and target genes using ChIP-seq in HeLa B2 cells.

2011-07-01 | GSE24518 | GEO

The activation of IL-1-induced enhancers depends on TAK1 kinase activity and NF-kappaB p65 I

Project description:The inflammatory gene response requires activation of the protein kinase TAK1, but it is currently unknown how TAK1-derived signals coordinate transcriptional programs in the genome. We determined the genome-wide binding of the TAK1-controlled NF-M-NM-:B subunit p65 in relation to active enhancers and promoters of transcribed genes by ChIP-seq experiments. Out of 35,000 active enhancer regions, 410 H3K4me1-positive enhancers show interleukin (IL)-1-induced H3K27ac and p65 binding. Inhibition of TAK1, IKK2 or depletion of p65 blocked inducible enhancer activation and gene expression. As exemplified by the CXC chemokine cluster located on chromosome 4, the TAK1-p65 pathway also regulates the recruitment kinetics of the histone acetyltransferase CBP, of NF-M-NM-:B p50 and of AP-1 transcription factors to both, promoters and enhancers. This study provides a high resolution view of epigenetic changes occurring during the IL-1 response and allows the first genome-wide identification of a novel class of inducible p65 NF-M-NM-:B-dependent enhancers in epithelial cells. Two sets of experiments were performed as biological replicate series (rep1 and rep2) each comprising of the following 4 conditions: Human epithelial KB cells were 1) left untreated or were 2) treated with Interleukin-1-alpha (10ng/M-BM-5l) for 1 hour, 3) treated for 1.5h with the TAK1 inhibitor 5Z-7-oxozeaenol (1M-BM-5M) or were 4) treated with 5Z-7-oxozeaenol for 30 minutes followed by Interleukin-1-alpha for 1 hour.

2014-12-17 | E-GEOD-64201 | biostudies-arrayexpress

Analysis of glucocorticoid receptor (NR3C1), NFkb (p65 subunit), and RNA polymerase 2 (RNAP2) binding in Beas-2B airway epithelial cells

Project description:The objective of this study was to determine binding patterns for GR, 65 and RNAP2 in Beas-2B airway epithelial cells after treatment with dexamethasone (100 nm), TNF (20 ng/ml) or both for one hour. This study utilized duplicate samples for each treatment condition and immunoprecipitation except for p65 immunoprcipitation of TNF treated samples, which was analyzed as a single sample. Input from vehicle treated cells was used a control. Experimental comparisons were made between the following samples/ treatment conditions. Duplicate samples of Beas-2B cells treated with ethanol (vehicle) were used for ChIP of GR, p65, and RNAP2 (2 samples each antibody). Duplicate samples of Beas-2B cells treated with dexamethasone were used for ChIP of GR and RNAP2 (2 samples each antibody). Duplicate samples of Beas-2B cells treated with TNF were used for ChIP of p65 and RNAP2 (1 sample p65, 2 samples RNAP2). Duplicate samples of Beas-2B cells treated with dexamethasone + TNF were used for ChIP of GR, p65 and RNAP2 (2 samples each antibody).

2016-04-01 | E-GEOD-79803 | biostudies-arrayexpress

Effect of cortisol on S. Typhimurium parental strain and an isogenic scsA mutant

Project description:S. Typhimurium 112910a parental strain and an isogenic M-NM-^TscsA strain were grown to stationary phase in SPI2 inducing minimal medium (MM5.8 - Erikkson et al., 2006 Inf & Imm., 74:1243) with or without supplementation with 1M-BM-5M cortisol 4 samples (stat phase wt, stat phase wt + 1M-BM-5M cortisol, stat phase M-NM-^TscsA, stat phase M-NM-^TscsA + 1M-BM-5M cortisol) and 3 biological replicates for each sample.

2014-02-28 | E-GEOD-55430 | biostudies-arrayexpress

Identifying the downstream effectors of E2F7 in squamous cell carcinoma (SCC) cells

Project description:Advanced head and neck squamous cell carcinomas (HNSCC) are frequently drug resistant and have a mortality rate of 40%. We have previously shown that E2F7 may contribute to drug sensitivity. In the present study, we conducted an M-bM-^@M-^Somics screen to identify factors that were responsible for E2F7-dependent resistance to anthracyclines by HNSCC. We provide, in vitro, in vivo and patient data that identifies the existence of a novel E2F7/Sphingosine kinase 1/Sphingosine-1-phosphate/AKT axis that regulates sensitivity to anthracyclines in HNSCC. Specifically, we show that E2F7-dependent sensitivity to doxorubicin occurs via induction of the sphingosine kinase 1/AKT axis. We also show that pharmacological inhibition of Sphingosine kinase 1 or AKT sensitizes SCC cells to the cytotoxic actions of doxorubicin in vitro and in vivo. Combined, these findings highlight a novel mechanism through which SCC cells acquire resistance to anthracyclines and identify specific pharmacological combinations that could be used to treat SCC. Duplicate total RNA isolated from i) untreated, KJD cells, ii) 1M-BM-5M doxorubicin-treated KJD cells, iii) control plasmid (pcDNA3) transfected, untreated KJD cells, iv) control plasmid (pcDNA3) transfected, 1M-BM-5M doxorubicin-treated KJD cells, v) E2F7 expression plasmid transfected, untreated KJD cells, vi) E2F7 expression plasmid transfected, 1M-BM-5M doxorubicin-treated KJD cells, vii) untreated, SCC25 cells, viii) 1M-BM-5M doxorubicin-treated SCC25 cells, ix) control siRNA (GFPsiRNA) transfected, untreated SCC25 cells, x) control siRNA (GFPsiRNA) transfected, 1M-BM-5M doxorubicin-treated SCC25 cells, xi) E2F7siRNA transfected, untreated SCC25 cells, xii) E2F7siRNA transfected, 1M-BM-5M doxorubicin-treated SCC25 cells were hybridised to an RNA microarray to identify genes which are downstream of E2F7 and regulate chemosensitivity in SCC.

2014-05-30 | E-GEOD-58074 | biostudies-arrayexpress

Identification and characterization of DNA sequences that restrict genomic binding of the glucocorticoid receptor

Project description:The glucocorticoid receptor (GR), is a hormone-activated transcription factor which binds to GR binding sequences (GBS) encoded in the genome. Interestingly, of the many genomic sequences matching the GR consensus sequence only a small subset is actually bound. This indicates that the presence of a GBS alone is insufficient to specify where in the genome GR binds. We identified sequences that can locally prevent GR binding and mass-spec analysis was used to identify proteins that bind to these sequences.

2016-03-30 | PXD002252 | Pride

Creation of an anti-inflammatory GR cistrome by TLR4 signaling

Project description:An unresolved molecular paradox is how the glucocorticoid receptor (GR) activates some genes while potently repressing others. We carried out genome-wide localization and expression profiling experiments in primary bone marrow-derived mouse macrophages treated with Dexamethasone in the presence or absence of LPS. Unexpectedly, we find that the anti-inflammatory GR cistrome, which is principally composed of 'canonical' GREs colocalizing with NFkB and AP-1 co-enriched with the myeloid lineage factors C/EBP and Pu.1, is shaped by TLR4-directed chromatin dynamics, suggesting that context rather than sequence may be a critical determinant of function. Identification of GR, cJun, NFkB(p65) binding sites in primary bone-marrow derived macrophages unstimulated and LPS-stimulated (3hrs) that were untreated or pre-treated with Dexamethasone for 16 hrs

2012-12-04 | E-GEOD-31796 | biostudies-arrayexpress

Transcription profiling of TCP10m-GR plants

Project description:Transgenic plants expressing a microRNA insensitive version of TCP10 (TCP10m) fused to the Glucocortocoid receptor (GR) in the jaw-D background and jaw-D mutants were grown for 21 days on MS agar. Nuclear import of TCP10m-GR was induced by transfer of plantlets to MS medium containing 10M-5M Dexamethasone and 10 M-5M Cycloheximide. The above ground parts of whole plantlets were harvested after 0, 2 and 4 hours.

2013-10-25 | E-TABM-1191 | biostudies-arrayexpress

Genome-wide profiling of Glucocorticoid receptor binding in A549, Nalm-6, MEF WT and MEF GCN5/PCAF double knockout (ChIP-seq)

Project description:To identify the sequences responsible for recruitment of Glucocorticoid receptor (GR) to individual loci, we performed ChIP-seq in four cell lines : A549 (ATTC:CCL-185), Nalm-6 (ATCC:CRL-1567), immortalized mouse embryonic fibroblasts (MEFs)(PMID 21131905), and immortalized PCAF-/-; GCN5flox/ MEFs (PMID 21131905) upon glucocorticoid treatment (1.5 hrs, 1M dexamethasone).

2016-11-10 | E-MTAB-5113 | biostudies-arrayexpress

Identification and validation of antisense RNAs in Escherichia coli

Project description:In this study transcriptional start sites (TSS) of E. coli were determined for several growth conditions To detect the complement of transcripts expressed from E. coli, we collected two independent biological replicates (B1 and B2 samples) from MG1655 wild type strain grown to exponential (OD 600 ~0.4) or stationary phase (OD 600 ~2.0) in LB medium (samples LB 0.4 and LB 2.0, respectively) as well as grown to exponential phase (OD 600 ~0.4) in M63 minimal glucose medium (sample M63 0.4). For all six samples, total RNA was extracted and subjected to differential RNA-seq (dRNA-seq) library preparation for primary transcriptome analysis as described previously (Sharma et al., 2010). Specifically, prior to cDNA library construction half of each RNA sample was treated with 5M-bM-^@M-^Y terminator exonuclease (+TEX samples), which degrades RNAs containing a 5M-bM-^@M-^Y-mono-phosphate (5M-bM-^@M-^Y-P) and, thus, enriching enriches for primary transcripts containing 5M-bM-^@M-^Y-tri-phosphates (5M-bM-^@M-^Y-PPP). The other half of each sample was left untreated (-TEX samples) and thus contains both primary transcripts (5M-bM-^@M-^Y-PPP) and processed RNAs (5M-bM-^@M-^Y-P).

2014-10-18 | E-GEOD-55199 | biostudies-arrayexpress

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