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Chip-chip from THP1 and HUVEC cells with ROR-alpha

ABSTRACT: ROR-alpha is a nuclear receptor, activity of which can be modulated by natural or synthetic ligands including cholesterol. Due to its possible involvement in, and potential therapeutic target for atherosclerosis, we aimed to identify ROR-alpha target genes in monocyte and endothelial cell lines, THP1 and HUVEC, respectively. ChIP-on-chip analysis of ROR-alpha demonstrated that ROR-alpha may target more than 3000 genes in monocytic and endothelial cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE94079 | GEO | 2017/02/28

SECONDARY ACCESSION(S): PRJNA368744

REPOSITORIES: GEO

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Homo sapiens

Project description:Chip-chip from THP1 and HUVEC cells with ROR-alpha

| PRJNA368744 | ENA

Expression data from interleukin-stimulated HUVEC

Project description:In the hematopoietic microenvironment, endothelial cells (ECs) play an important role in the regulation of hematopoietic cell proliferation and trafficking. We previously demonstrated that EC stimulated with tumor necrosis factor alpha (TNF-α) induce the generation of dendritic cells from CD34(+) stem cells, whereas in contrast, interleukins were capable of inducing the proliferation of hematopoietic and myeloid progenitors. In order to identify potentially new soluble factors which greatly impact the self-renewal, proliferation and differentiation of CD34+ hematopoietic stem cells (HSC), we examined the expression profiles of IL-1ß, IL-3 and IL-6 stimulated human umbilical vein endothelial cells (HUVEC).

2011-07-01 | GSE22325 | GEO

ATAC-seq of Thp1-mono, Thp1-macro, and Thp1-M.tb

Project description:Next Generation Sequencing data of ATAC-Seq library of Thp1-mono, Thp1-macro, and Thp1-M.tb

2022-09-06 | GSE208044 | GEO

ChIP-seq of Thp1-mono, Thp1-macro, and Thp1-M.tb

Project description:Next Generation Sequencing data of ChIP-seq library of Thp1-mono, Thp1-macro, and Thp1-M.tb

2022-09-06 | GSE208043 | GEO

Chemical Inhibition of the ROR?t-dependent Transcriptional Network in Th17 cells [RNA-Seq]

Project description:ROR?t is a transcription factor required for T helper 17 (Th17) cell development. We identified three ROR?t-specific inhibitors that suppress Th17 cell responses including Th17 cell-mediated autoimmune disease. We systemically characterized ROR?t binding data in the presence and absence of drug with corresponding whole-transcriptome sequencing for wild-type and ROR?t-deficient cells. ROR?t is central in a densely interconnected regulatory network, acting both as a direct activator of genes important for Th17 cell differentiation and as a direct repressor of genes from other T-cell lineages. The three inhibitors identified here reversed both of these modes of action, but to varying extents and through distinct mechanisms. Whereas one inhibitor displaced ROR?t from its target-loci, the two more potent inhibitors affected transcription predominantly without removing DNA-binding. Our work illustrates the power of a system-scale analysis of transcriptional regulation to characterize potential therapeutic compounds that inhibit pathogenic Th17 cells and suppress autoimmunity. Transcriptional profiling of Th17 cells under chemical perturbations of ROR?t, DMSO, and knockout of ROR?t

2014-04-17 | E-GEOD-56018 | biostudies-arrayexpress

ROR-γ drives androgen-receptor expression and represents a therapeutic target in castration-resistant prostate cancer

Project description:The androgen receptor (AR) is overexpressed and hyperactivated in human castration-resistant prostate cancer (CRPC). However, the determinants of AR overexpression in CRPC are poorly defined. Here we show that retinoic acid receptor–related orphan receptor γ (ROR-γ) is overexpressed and amplified in metastatic CRPC tumors, and that ROR-γ drives AR expression in the tumors. ROR-γ recruits nuclear receptor coactivator 1 and 3 (NCOA1 and NCOA3, also known as SRC-1 and SRC-3) to an AR–ROR response element (RORE) to stimulate AR gene transcription. ROR-γ antagonists suppress the expression of both AR and its variant AR-V7 in prostate cancer (PCa) cell lines and tumors. ROR-γ antagonists also markedly diminish genome-wide AR binding, H3K27ac abundance and expression of the AR target gene network. Finally, ROR-γ antagonists suppressed tumor growth in multiple AR-expressing, but not AR-negative, xenograft PCa models, and they effectively sensitized CRPC tumors to enzalutamide, without overt toxicity in mice. Taken together, these results establish ROR-γ as a key player in CRPC by acting upstream of AR and as a potential therapeutic target for advanced PCa.

2016-03-08 | GSE72714 | GEO

ROR-γ drives androgen-receptor expression and represents a therapeutic target in castration-resistant prostate cancer

2016-03-08 | GSE72483 | GEO

miRNA in HUVEC culture supernatant

Project description:Human umbilical vein endothelial cells (HUVEC) were cultured in serum-free medium with 50 μmol/L ADMA (ADMA group) or without ADMA (NA group ). Asymmetric dimethylarginine is a typical uremic toxin which used to induce HUVEC injury.

2022-07-05 | GSE207436 | GEO

SUMOylation of ROR-gt inhibit IL-17 expression and inflamatiion

Project description:RNA sequencing of ROR-gt-/- mouse-derived T cells reconstituted with either WT-ROR-gt or mutant (SUMOylation-defective ROR-gt)

2018-10-12 | GSE116407 | GEO

ROR-Î³ drives androgen-receptor expression and represents a therapeutic target in castration-resistant prostate cancer

Project description:The androgen receptor (AR) is overexpressed and hyperactivated in human castration-resistant prostate cancer (CRPC). However, the determinants of AR overexpression in CRPC are poorly defined. Here we show that retinoic acid receptorârelated orphan receptor Î³ (ROR-Î³) is overexpressed and amplified in metastatic CRPC tumors, and that ROR-Î³ drives AR expression in the tumors. ROR-Î³ recruits nuclear receptor coactivator 1 and 3 (NCOA1 and NCOA3, also known as SRC-1 and SRC-3) to an ARâROR response element (RORE) to stimulate AR gene transcription. ROR-Î³ antagonists suppress the expression of both AR and its variant AR-V7 in prostate cancer (PCa) cell lines and tumors. ROR-Î³ antagonists also markedly diminish genome-wide AR binding, H3K27ac abundance and expression of the AR target gene network. Finally, ROR-Î³ antagonists suppressed tumor growth in multiple AR-expressing, but not AR-negative, xenograft PCa models, and they effectively sensitized CRPC tumors to enzalutamide, without overt toxicity in mice. Taken together, these results establish ROR-Î³ as a key player in CRPC by acting upstream of AR and as a potential therapeutic target for advanced PCa. A total of 16 samples were analyzed in this study. The study included one cell line C4-2B. C4-2B cells were cultured in medium containing vehicle control or SR2211 (5 ÂµM) for 24 hours, cells then were collected for ChIP seq assay

2016-03-08 | E-GEOD-72714 | biostudies-arrayexpress

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