Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cardiac microarray changes in a transgenic mouse expressing a human mitochondrial progesterone receptor (PR-M).

ABSTRACT: Cardiac microarray changes in a transgenic mouse expressing a human mitochondrial progesterone receptor (PR-M).

PROVIDER: PRJNA427599 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Cardiac microarray changes in a transgenic mouse expressing a human mitochondrial progesterone receptor (PR-M).

Project description:A TET-On transgenic mouse model was develop for cardiac expression of a human mitochondrial progesterone receptor (PR-M). Expression was verified by immunohistochemistry and RT-PCR. Previous research with cell knockdown and overexpression has shown a ligand dependent increase in cellular respiration with this receptor. Mice expressing (N=3) or not expressing (N=3) PR-M were treated with progesterone for 19-21 days prior to sacrifice. Tissue from the apical cardiac ventrical was submitted for microarray.

2017-12-27 | GSE108551 | GEO

Genome-wide mapping of ligand-dependent progesterone receptor chromatin interactions in human breast cell lines using PR ChIP-seq

2012-04-26 | GSE31129 | GEO

Title: Site specific O-GlcNAcylation of progesterone receptor (PR) supports PR attenuation of interferon stimulated genes (ISGs) and tumor growth in breast cancer

Project description:Hormone receptor (HR) positive breast cancer, defined by expression of estrogen (ER) and/or progesterone (PR) receptor expression, is the most commonly diagnosed type of breast cancer. PR alters the transcriptional landscape to support tumor growth in concert with or independent of ER. Understanding the mechanisms regulating PR function are critical to developing new strategies to treat HR+ breast cancer. O-GlcNAc is a post-translational modification responsible for nutrient sensing that fine tunes protein function. We have previously reported O-GlcNAcylation on PR. Although PR is heavily post translationally modified, primarily through phosphorylation, specific sites of O-GlcNAcylation on PR, and how they regulate PR action, have not been investigated. Using established PR-expressing breast cancer cell lines, we mapped the sites of O-GlcNAcylation on PR. RNA-sequencing revealed site-specific O-GlcNAcylation of PR is critical for ligand-independent suppression of interferon signaling, a regulatory function of PR previously studied in our lab. Furthermore, O-GlcNAcylation of PR enhances PR-driven tumor growth in vivo. We have delineated one mechanism regulating PR function in breast cancer that impacts tumor growth, and provided additional insight into the mechanism through which PR attenuates interferon signaling.

2024-06-17 | MSV000095057 | MassIVE

Mechanism of Telapristone acetate (TPA) on Progesterone receptor (PR) action in T47D breast cancer cells

Project description:To obtain a global analysis of the effect of TPA on the Progesterone Receptor (PR) cistrome

2018-12-26 | GSE113607 | GEO

Genome-wide mapping of ligand-dependent progesterone receptor chromatin interactions in human breast cell lines using PR ChIP-seq

Project description:The effects of progesterone are pleiotropic, resulting in diverse outcomes in a range of target tissues. Progesterone signalling is mediated through the nuclear progesterone receptor (PR) and to identify whether the cell specificity of the PR transcriptome arises from distinct patterns of genomic interaction of PR, we have mapped the genomic binding sites for PR in breast cancer cells and minimally transformed breast cells. PR binding was correlated with transcriptional outcome in both cell lines. Three replicate PR ChIP samples and two replicate input DNA control samples from T-47D breast cancer cells and two replicate PR ChIP samples and two replicate input DNA control samples from AB32 transformed normal breast cells.

2012-04-25 | E-GEOD-31129 | biostudies-arrayexpress

Selective suppression of endothelial cytokine production by progesterone receptor [RNA-seq]

Project description:Steroid hormones are well-recognized suppressors of the inflammatory response, however, their cell- and tissue-specific effects in the regulation of inflammation are far less understood, particularly for the sex-related steroids. To determine the contribution of progesterone in the endothelium, we have characterized and validated an in vitro culture system in which human umbilical vein endothelial cells constitutively express human progesterone receptor (PR). Using next generation RNA-sequencing, we identified a selective group of cytokines that are suppressed by progesterone both under physiological conditions and during pathological activation by lipopolysaccharide. In particular, IL-6, IL-8, CXCL2/3, and CXCL1 were found to be direct targets of PR, as determined by ChIP-sequencing. Regulation of these cytokines by progesterone was also confirmed by bead-based multiplex cytokine assays and quantitative PCR. These findings provide a novel role for PR in the direct regulation of cytokine levels secreted by the endothelium. They also suggest that progesterone-PR signaling in the endothelium directly impacts leukocyte trafficking in PR-expressing tissues Examination of PR target genes in human umbilical vein endothelial cells (HUVECs) using RNA-seq PR infected only (PR); PR infected followed by ligand treatment (PR+P); PR infected followed by 4h LPS treatment (PR+LPs_4h); PR infected followed by 8h LPS treatment (PR+LPs_8h); PR infected followed by 4h LPS and progesterone treatment (PR+LPS+P_4h); PR infected followed by 8h LPS and progesterone treatment (PR+LPS+P_8h)

2014-01-01 | E-GEOD-46502 | biostudies-arrayexpress

Phosphorylated and Sumoylation-Deficient Progesterone Receptors Drive Proliferative Gene Signatures During Breast Cancer Progression (Affymetrix gene expression analysis)

Project description:Anlaysis of the differential gene expression between T47D cells expressing wild type (WT) progesterone receptor isoform B (PR) or SUMOylation-deficient PR molecules.

2012-06-07 | GSE34147 | GEO

Phosphorylated and Sumoylation-Deficient Progesterone Receptors Drive Proliferative Gene Signatures During Breast Cancer Progression (Illumina gene expression analysis)

Project description:Anlaysis of the differential gene expression between T47D cells expressing wild type (WT) progesterone receptor isoform B (PR) or SUMOylation-deficient PR molecules.

2012-06-07 | GSE34148 | GEO

Differential regulation of SGK1 by progesterone activates AP-1/NDRG1 genomic axis in PR-positive and negative breast cancer cells

Project description:Pre-operative progesterone intervention has been shown to confer a survival benefit to breast cancer patients independent of their progesterone receptor (PR) status, raising a question about how progesterone affects the outcome of PR-negative cells. Here, we identify up-regulation of a Serum- and glucocorticoid-regulated kinase gene, SGK1 and an N-Myc Downstream Regulated Gene 1, NDRG1, along with down-regulation of miR-29a and miR-101-1 targeting 3’UTR region of SGK1, to differential extents in a PR dependent manner in breast cancer cells. We further demonstrate a novel dual-phase transcriptional and post-transcriptional regulation of SGK1 in response to progesterone leading to up-regulation of a tumor metastasis suppressor gene, NDRG1, mediated by a set of AP-1 network genes. The NDRG1 further inactivates a set of kinases impeding the invasion and migration of breast cancer cells. In summary, we propose a model for the mode of action of progesterone in breast cancer deciphering the molecular basis of a randomized clinical trial studying the effect of progesterone in breast cancer with a potential to improve the prognosis of breast cancer patients for receiving pre-operative progesterone treatment.

2018-10-19 | E-MTAB-6742 | biostudies-arrayexpress

Selective suppression of endothelial cytokine production by progesterone receptor [RNA-seq]

2014-01-01 | GSE46502 | GEO