Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA121131 | ENA |
REPOSITORIES: ENA
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Project description:Retinoic acid receptor-related orphan receptor α regulates bystander activation of memory CD8+ T cells
| PRJNA1300295 | ENA
Project description:Retinoic acid receptor-related orphan receptor α regulates bystander activation of memory CD8+ T cells [RNA-Seq]
| PRJNA1299279 | ENA
Project description:Retinoic acid-related Orphan Receptor alpha (RORalpha; NR1F1) is a nuclear receptor involved in several physiological and patho-physiological functions including lipid metabolism, inflammation, angiogenesis, and circadian rythm. It is widely distributed. In order to better understand the role of this nuclear receptor in liver, we aimed at displaying genes controlled by RORalpha in liver cells. HepG2 human hepatoma cells stably over-expressing RORalpha were designed. Genes whose expression was altered in these cells versus control cells were displayed using micro-arrays and qRT-PCR. Expression of these genes was also altered in cells in which RORalpha was transiently over-expressed after adenoviral infection. Some genes are involved in functions controlled by RORalpha. This is the case for LPA, NR1D2 and ADIPOQ in lipid metabolism, ADIPOQ and PLG in inflammation, PLG in fibrinolysis and NR1D2 and NR1D1 in circadian rhythm. This study also revealed that genes such as G6PC, involved in glucose homeostasis, and AGRP, involved in the control of body weight, are also controlled by RORalpha. Lastly, SPARC, involved in cell growth and adhesion and associated with liver carcinogenesis, was up-regulated by RORalpha. It is a new direct RORalpha target gene since it possesses, in its promoter, a functional RORE as evidenced by EMSAs and transfection experiments. It is likely the case for most of the other genes we found regulated by RORalpha contain putative ROREs in their regulatory regions. These results open new routes to think about the role of RORalpha in glucose metabolism and carcinogenesis within cells of hepatic origin. Keywords: Comparison of HepG2 cells expressing RORalpha or control HepG2 cells cultured in 20% oxygen or 2% oxygen during 24h.
2009-11-04 | GSE18875 | GEO
Project description:Identification and validation of the pathways and functions regulated by the orphan nuclear receptor, ROR alpha1, in skeletal muscle The retinoic acid receptor-related orphan receptor (ROR) alpha has been demonstrated to regulate lipid metabolism. We were interested in the physiologically relevant roles, and pathways regulated by RORalpha1 action in skeletal muscle. This major mass organ accounts for ~40% of the total body mass, and significant levels of lipid catabolism, glucose disposal and energy expenditure. We utilized the strategy of targeted muscle specific expression of a truncated (dominant negative) RORalphaâDE in transgenic mice, to investigate RORalpha1 signalling (and function) in this peripheral tissue. Expression profiling and pathway analysis indicated that RORalpha regulated genes involved in: (i) lipid and carbohydrate metabolism, cardiovascular and metabolic disease; and (ii) the LXR nuclear receptor signaling pathway and, (iii) the Akt and AMPK signaling cascades. This analysis was extensively validated by rigorous qPCR analysis using TaqMan Low Density Arrays, coupled to rigorous statistical analysis (with Empirical Bayes, and Benjamini-Hochberg). Moreover, westerns and metabolic profiling were utilized to validate the genes, proteins and pathways (lipogenic, Akt, AMPK and fatty acid oxidation) involved in the regulation of metabolism by RORalph1. The identified genes and pathways were in concordance with the demonstration of hyperglycemia, glucose intolerance, attenuated insulin stimulated phosphorylation of Akt, and impaired glucose uptake in the transgenic heterozygous Tg-RORalphaâDE animals. In conclusion, we propose that RORalpha1 is involved in regulating the Akt2-AMPK signalling pathways in the context of lipid homeostasis in skeletal muscle. Total RNA was compared from quadriceps femoris of both transgenic and wild type mice. Transgenic mice contained a truncated version of human RORalpha1 (RORalpha1delDE) where the entire E region and part of the hinge/D region have been removed. This transgene is driven by a skeletal muscle specific human skeletal alpha-actin (HSA) promoter.
2010-04-13 | E-GEOD-20646 | biostudies-arrayexpress
Project description:The retinoic acid receptor-related orphan receptor a (RORa) is a member of the NR1 subfamily of orphan nuclear hormone receptors. RORa is an important regulator of various biological processes, including cerebellum development, cancer and circadian rhythm. To determine molecular mechanism by which hepatic deletion of RORa induces obesity and insulin resistance, we performed global transcriptome analysis from high-fat diet (HFD)-fed RORa f/f and RORa LKO mouse liver tissues. This analysis provides insight into molecular mechanisms for RORa in high-fat-diet condition.
2017-06-28 | GSE83338 | GEO
Project description:About one-third of oestrogen receptor alpha- positive breast cancer patients treated with tamoxifen relapse. Here we identify the nuclear receptor retinoic acid receptor alpha as a marker of tamoxifen resistance. Using quantitative mass spectrometry-based proteomics, we show that retinoic acid receptor alpha protein networks and levels differ in a tamoxifen-sensitive (MCF7) and a tamoxifen-resistant (LCC2) cell line. High intratumoural retinoic acid receptor alpha protein levels also correlate with reduced relapse-free survival in oestrogen receptor alpha-positive breast cancer patients treated with adjuvant tamoxifen solely. A similar retinoic acid receptor alpha expression pattern is seen in a comparable independent patient cohort. An oestrogen receptor alpha and retinoic acid receptor alpha ligand screening reveals that tamoxifen-resistant LCC2 cells have increased sensitivity to retinoic acid receptor alpha ligands and are less sensitive to oestrogen receptor alpha ligands compared with MCF7 cells. Our data indicate that retinoic acid receptor alpha may be a novel therapeutic target and a predictive factor for oestrogen receptor alpha-positive breast cancer patients treated with adjuvant tamoxifen. Peptide and protein identification data set 1: Peptide identification from the MALDI-TOF/TOF data was carried out using the Paragon algorithm in the ProteinPilot 2.0 software package (Applied Biosystems) 46. Default settings for a 4800 instrument were used (i.e., no manual settings for mass tolerance was given). The following parameters were selected in the analysis method: iTRAQ 4plex peptide labelled as sample type, MMTS as alkylating agent of cysteine, trypsin as digesting enzyme, 4800 as instrument, gel based ID and Urea denaturation as special factors, biological modifications as ID focus, and thorough ID as search effort. Peptide identification from the Q-TOF data was carried out using the Spectrum Mill Protein Identification software (Agilent). Data was extracted between MH+ 600 and 4000 Da (Agilent's definition). Scans with the same precursor m/z 90 sec, 0.05 m/z matching with a minimum of 20 peaks in MS2 were merged. Peptide and protein identification data set 2: Proteome discoverer 1.3 with sequest-percolator was used for protein identification. Precursor mass tolerance was set to 10 ppm and for fragments 0.8 Da and 0.02 Da were used for detection in the linear iontrap and the orbitrap, respectively. Oxidized methionine and phosphorylation on S,T and Y was set as dynamic modifications, and carbamidomethylation, N-terminal 8plex iTRAQ, and lysyl 8plex iTRAQ as fixed modifications. Spectra were matched to ensembl 68 limited to human protein sequences, and results were filtered to 1% FDR.
2013-07-24 | PXD000281 | Pride
Project description:Retinoic Acid Related Receptor Orphan Receptor a (RORa) expressing T regulatory cells thwart type-2 cutaneous allergic inflammation
| PRJNA387247 | ENA
Project description:Cistrome profiles of Retinoids x Receptor alpha (RXRα) , Retinoic Acid Receptor alpha (RARα), and Retinoic Acid Receptor beta (RARβ) in livers of mice treated by control and retionic acid-containing diet
| PRJNA232748 | ENA
Project description:We developed genetically engineered HepG2/8F_HS cells, in which eight liver-enriched transcription factor (LETF) genes—hepatocyte nuclear factor (HNF)-1α, HNF-1β, HNF-3β, HNF-4α, HNF-6, CCAAT/enhancer binding protein (C/EBP)-α, C/EBP-β and C/EBP-γ— under the control of TRE/PCMVmin promoter were introduced into a previously developed human hepatoma cell line (HepG2-HSP). The heat-inducible synthetic promoter system was introduced into HepG2 cells and tetracycline-responsive transactivator (tTA) and enhanced green fluorescent protein (EGFP) were expressed via positive feedback of tTA transcription in response to heat treatment. HepG2/8F_HS cells can induce high liver functions by heat treatment via overexpression of LETF genes.
2022-04-04 | E-MTAB-11486 | biostudies-arrayexpress
Project description:In the current study we have generated a CRISPR-Cas9 mediated SVIP knockout rat hepatoma cell line with the goal to further understand the functional role of SVIP in the complex process of VLDL transport and secretion. We observed that complete absence of SVIP protein results in enhanced retention of VLDL in the hepatoma cells. This was marked by both an increased expression of apoB100 protein and neutral lipid staining detected inside SVIP knockout (SVIP KO) cells. Furthermore, RNA sequencing studies of the SVIP KO hepatoma cells revealed a significant downregulation of genes within the peroxisome proliferator- activated receptor alpha (PPAR alpha) and the nuclear factor erythroid 2-related factor 2 (Nrf2) pathways, thereby affecting hepatic fatty acid (FA) metabolism. Most importantly, we observed that cells lacking SVIP demonstrated a substantial down regulation of another very important gene associated with FA metabolism, namely the liver fatty acid-binding protein (L-FABP). Additionally, the RNAseq data also reveals that the loss of SVIP thrusts the hepatoma cells into an acute phase response (APR) like state, with an increase in the expression of protein synthesis genes.
2025-08-20 | GSE289707 | GEO