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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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE24518 | GEO | 2011/07/01

SECONDARY ACCESSION(S): PRJNA132601

REPOSITORIES: GEO

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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. 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

2011-07-01 | E-GEOD-24518 | biostudies-arrayexpress

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Project description:p65-/-Ras cells show delayed tumor formation in SCID mice. However, after prolonged latency, tumor formation was observed from these mice. To understand the changes of NF-kB regulated genes before and after tumor formation, RNA from p65+/+Ras, p65+/+RasTumor, p65-/-Ras, p65-/-RasTumor cells were isolated and microarray were performed. p65+/+Ras and p65-/-Ras cells were injected into SCID mice. Tumors were removed and put back into tissue culture. RNA was isolated from these cells and microarrays were performed.

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GR HeLa ChIP-seq

Project description:GR HeLa ChIP-seq

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NF-kB in Tumor Initiation

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Project description:Chromatin immunoprecipitation using GR antibodies in HeLa cells detected by Illumina sequencing

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Project description:Purpose: The glucocorticoid receptor is widely expressed across mutliple tissues, and yet has very tissue specfic actions. This is most likely due to the tissue specific chormatin landscape which dictates GR binding. It identify GR tragets in myeloma as potential therapeutic targets, we have used ChIP-seq to identify myeloma specific GR binding sites. Methods: DNA-chromatin complexes were isolated from MM.1S (GR positive) or MM.1RL (GR negative) cells following a 2 hour treatment with either 1 micromolar dexamethasone or vehicle control. Complexes were immunoprecipitated with either a GR specific antibody or an IgG control and the DNA isolated for next generation sequencing. Results: We identified 8689 high confidence GR binding sites and further correlated those sites to specific genes which are regulated by glucocorticoids through integration with gene expression array data from our lab (submitted to GEO speparately). Conclusions: Overall, our results indentified nearly 400 genes under the direct transcriptional control of glucocorticoids in myeloma cells.

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Ribosomal protein S3: a functional component of NF-kB p65 binding complexes

Project description:To explore the effects on the NF-kB transcriptome after knockdown of RPS3 in stimulated T cells, we performed microarray assays comparing RPS3-silenced versus NS-treated samples on the same chip. p65-silenced versus NS-treated samples were used as a control. Keywords: time series design Jurkat cells transfected with control siRNA versus RPS3 or p65-siRNA were stimuated with TCR for 1, 3, or 6 hours for a total of 6 arrays.

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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

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An NF-kB-dependent, lineage specific transcriptional program regulates Treg identity and function [ChIP-seq]

Project description:NF-kB p65 ChIPseq revealed differential binding of p65 in Treg vs Tconv upon TCR stimulation

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