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NR2F2 genome occupancy and the H3K4me1 histone mark profile in the mouse uterus at gestation day 3.5

ABSTRACT: NR2F2 genome occupancy and H3K4me1 histone mark profiles in the prereceptive stage of the pregnant mouse uterine specimens were documented by ChIP-seq to investigate downstream targets of the NR2F2 and candidate partner transcription regulators.

ORGANISM(S): Mus musculus

PROVIDER: GSE232582 | GEO | 2023/08/03

REPOSITORIES: GEO

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Nr2f2 deficiency in Pgr-expressing cells; NR2F2 genome occupancy and the H3K4me1 histone mark; uterus at gestation day 3.5

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-03 | GSE232583 | GEO

PGR genome occupancy and the H3K27ac histone mark profile in mouse uteri at gestation day 13

Project description:PGR genome occupancy and H3K27ac histone mark profiles in pregnant mouse uterine specimens were documented by ChIP-seq to investigate downstream targets of the progesterone receptor and candidate partner transcription regulators.

2022-09-21 | GSE199099 | GEO

Uterine transcriptomic profiles of Nr2f2 deficiency in Pgr-expressing cells at gestation day 3.5

Project description:Endometrial epithelia and stroma communicate via progesterone and estrogen signaling to prepare a receptive uterus for embryo implantation in early pregnancy. The present study determines, in early pregnancy at the prereceptive stage, the uterine gene signature of the NR2F2 transcription factor that is crucial for mediating the progesterone dependent anti-proliferative actions in the epithelia.

2023-08-03 | GSE232580 | GEO

NR2F2 study

Project description:NR2F2 study

| PRJNA548079 | ENA

Expression and functional pathway analysis of nuclear receptor NR2F2 in Ovarian cancer

Project description:Analysis of NR2F2 knockdown at whole genome level Total RNA isolated 48 hours after NR2F2 knockdown with siRNA compared to siRNA with non-targeting control

2013-05-29 | E-GEOD-47438 | biostudies-arrayexpress

Comparative analysis of RNA-seq data from human ALT+ cell lines treated with NR2F2 siRNA

Project description:The Alternative Lengthening of Telomeres (ALT) facilitates telomere lengthening by a DNA strand invasion and copying mechanism. The nuclear receptor NR2F2 can bind to (TCAGGG)n variant repeats within telomeres and it has been proposed that this facilitates telomere interactions in ALT+ cells. However, the role NR2F2 in regulation the gene expression in ALT+ cell lines is unclear. Here, using Next Generation Sequencing (NGS), we characterised the changes in expression profile of three ALT+ cell lines (W-V, WI38VA13/2RA, U2OS) upon transient siRNA mediated downregulation of NR2F2 compared to cells treated with a control siRNA . Among 86 ALT-associated genes, only MND1 showed consistent down-regulation across the three NR2F2-depleted ALT+ cell lines. Altogether our data indicate that NR2F2 it does not play a direct role in the ALT mechanism.

2020-12-15 | E-MTAB-9599 | biostudies-arrayexpress

RNAi profiling of human lymphatic endothelial cells after knockdown of Prox1 and/or NR2F2

Project description:Gene expression profiles of primary lymphatic endothelial cells (LECs) isolated from human foreskin were analyzed after siRNA-mediated knockdown of control (firefly luciferase), Prox1, NR2F2 or Prox1/NR2F2 for 48 hours. Experiment Overall Design: Passage five human lymphatic endothelial cells (LECs) were cultured on fibronectin (10 Î¼g/ml)-coated plates in a complete media (EBM, 20% FBS supplemented with 10 Î¼g/ml hydrocortisone acetate, 25 ug/ml cAMP and antibiotics). LECs were harvested and electorporated with siRNA duplexes for 48 hours with siRNA duplexes against either firefly luciferase(control), Prox1, NR2F2 or Prox1/NR2F2. Total RNA was purified using Tri-reagent and was subjected to microarray analysis. Experiment Overall Design:

2008-10-25 | E-GEOD-12846 | biostudies-arrayexpress

Endothelial dysfunction in NR2F2-silenced cells - EA.hy926 cells model

Project description:Orphan nuclear receptor chicken ovalbumin upstream promoter transcription factor 2 (COUPTF2; NR2F2) is highly expressed in endothelial cells (ECs) and Nr2f2 knockout produces lethal cardiovascular defects. In humans, NR2F2 mutations result in both congenital heart disease and diaphragmatic hernia, conditions associated with the development of pulmonary arterial hypertension (PAH). However, COUPTF2 functions in mature endothelium are uncertain. NR2F2 knockdown in primary human endothelial cells (ECs) led to an interferon-biased inflammatory response, endothelial-to-mesenchymal transition, proliferation, hypermigration, apoptosis-resistance and mitochondrial dysfunction. These phenotypic changes were associated with AKT activation and increased Dickkopf-1 (DKK1) expression, a Wnt/β-catenin pathway inhibitor. DKK1 was also elevated in patients with PAH and secreted in response to loss of bone morphogenetic receptor type 2 (BMPR2), the archetypal PAH-associated genetic defect. Together, these findings demonstrate that endothelial NR2F2 suppresses inflammation and proliferation. Thus, NR2F2 loss disrupts EC homeostasis and may promote pathologic vascular remodeling in the development of PAH.

2023-05-31 | GSE188465 | GEO

NR2F2 ChIP-sequencing of melanoma cell lines

Project description:Melanoma is a highly metastatic tumor type responsible of the large majority of the skin cancer-related deaths. Melanoma cells recapitulate the migratory and invasive nature of neural crest stem cells from which melanocytes arise. However, the mechanisms by which these developmental programs confer melanoma cells with more aggressive properties are not understood. Here we provide evidence for an epigenetically regulated developmental program that is aberrantly re-activated by melanoma cells to aid in the metastatic process. We reasoned that studying molecular changes occurring during the ontogeny of melanocytes from progenitor neural crest cells (NCC), and identifying developmental programs retained or re-gained by melanoma cells, could reveal crucial processes that modulate melanoma aggressiveness. Here we describe a novel mechanism that controls the activity of a transcriptional regulator of human neural crest, the Nuclear Receptor Subfamily 2 Group F, Member 2 (NR2F2). We find that highly localized DNA methylation acts as an on/off switch that controls the expression of a truncated NR2F2 isoform (NR2F2-Iso2) from an alternative transcription start site during NCC to melanocyte differentiation. We show that melanoma cells co-opt this developmental program by decreased DNA methylation and re-expression of NR2F2-Iso2 to promote melanoma metastasis. NR2F2-Iso2 regulates the transcriptional activity of the full length NR2F2 isoform 1 by impairing its binding to chromatin, which results in altered expression of NCC and differentiation genes. Our data demonstrate that epigenetic reactivation of NR2F2 isoform 2 promotes melanoma metastasis, which could be targeted for therapeutic purposes.

2023-02-12 | GSE102552 | GEO

Differential chromatine state and ER binding potentially induced by NR2F2 depletion.

Project description:ERα binding activity largely depends on access to binding sites on chromatin, which is facilitated in part by Pioneer Factors (PFs).We show that most binding events of NR2F2 occur together with the ERα binding sites.To explore whether NR2F2 may act as potential pioneer factor of ER, we performed a series of ChIP-seq genome wide in MCF-7. Since NR2F2 associates with chromatin prior to estrogen treatment and its depletion in MCF-7 cells did not affect ERα expression, we hypothesize NR2F2 may inhibit estrogen-dependent growth by modulating ERα recruitment. We performed ChIP-seq genome wide gainst ERα before and after NR2F2 depletion.Covalent modifications are a main chromatin property.To test whether NR2F2 favoured histone modification deposition on chromatin, we profiled ChIP-Seq of H3K4me1, H3K4me3, and H3K27ac following NR2F2 depletion in oestrogen-starved MCF-7 cells to gain comprehensive histone medication landscape.

2019-10-15 | GSE132432 | GEO

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