Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE120851
PROVIDER: PRJNA377914 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5312360_1.fastq.gz | Fastqsanger.gz | |||
| SRR5312360_2.fastq.gz | Fastqsanger.gz | |||
| SRR5312370_1.fastq.gz | Fastqsanger.gz | |||
| SRR5312370_2.fastq.gz | Fastqsanger.gz | |||
| SRR5312361_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 44 |
Similar Datasets
Project description:Changes in gene expression were assayed in mouse liver nuclear RNA following a single injection of the CAR agonist TCPOBOP (1,4-Bis-[2-(3,5-dichloropyridyloxy)]benzene) or the PXR agonist PCN (pregnenolone 16α-carbonitrile) in 7-week old mice. This study is part of a larger study entitled Sex-Differential Responses of Tumor Promotion-Associated Genes and Dysregulation of Novel Long Noncoding RNAs in Constitutive Androstane Receptor-Activated Mouse Liver (PMID: 28903501).
2017-07-14 | GSE95685 | GEO
Project description:Modulation of the mouse liver epigenome following TCPOBOP exposure
| PRJNA408126 | ENA
Project description:TCPOBOP (1,4-bis[2-(3,5-dichloropyridyloxy)]benzene) and PCN (pregnenolone 16α-carbonitrile) are inducers of drug metabolism through activation of nuclear receptors CAR (constitutive androstane receptor) and PXR (pregnane X receptor), respectively. Mouse experiment was designed to study the effect of CAR and PXR activation on cholesterol homeostasis genes and other genes, which are present on the Steroltalk v2 microarray. Treatments were combined with standard and high-cholesterol diet to observe the interference of high liver cholesterol on nuclear receptor transcription regulation. All experiments were done within the European sixth Framework program âSteroltalkâ (www.steroltalk.net). Results form these experiments give new knowledge about involvement of âxenosensorsâ CAR and PXR in regulation of endogenous liver metabolism. Animals were injected i.p. 3mg/kg TCPOBOP, 40 mg/kg PCN or vehicle (corn oil) in combination of one week of standard or 1% cholesterol diet prior tretament. After 24h they were sacrificed and total RNA was isolated from the livers. Each sample was hybridized with a reference sample to Steroltalk v2 microarrays.
2010-10-08 | E-GEOD-13688 | biostudies-arrayexpress
Project description:Changes in chromatin accessibility in mouse liver following TCPOBOP exposure
| PRJNA408131 | ENA
Project description:Sex differences in liver gene expression are dictated by sex-differences in circulating growth hormone (GH) profiles. Presently, the pituitary hormone dependence of mouse liver gene expression was investigated on a global scale to discover sex-specific early GH response genes that might contribute to sex-specific regulation of downstream GH targets and to ascertain whether intrinsic sex-differences characterize hepatic responses to plasma GH stimulation. RNA expression analysis using 41,000-feature microarrays revealed two distinct classes of sex-specific mouse liver genes: genes subject to positive regulation (class-I) and genes subject to negative regulation by pituitary hormones (class-II). Genes activated or repressed in hypophysectomized (Hypox) mouse liver within 30-90min of GH pulse treatment at a physiological dose were identified as direct targets of GH action (early response genes). Intrinsic sex-differences in the GH responsiveness of a subset of these early response genes were observed. Notably, 45 male-specific genes, including five encoding transcriptional regulators that may mediate downstream sex-specific transcriptional responses, were rapidly induced by GH (within 30min) in Hypox male but not Hypox female mouse liver. The early GH response genes were enriched in 29 male-specific targets of the transcription factor Mef2, whose activation in hepatic stellate cells is associated with liver fibrosis leading to hepatocellular carcinoma, a male-predominant disease. Thus, the rapid activation by GH pulses of certain sex-specific genes is modulated by intrinsic sex-specific factors, which may be associated with prior hormone exposure (epigenetic mechanisms) or genetic factors that are pituitary-independent, and could contribute to sex-differences in predisposition to liver cancer or other hepatic pathophysiologies.
2010-01-27 | GSE17644 | GEO
Project description:RNA-seq data of mouse liver treated with TCPOBOP
| PRJNA420496 | ENA
Project description:PolyA-selected RNA was isolated from the nuclear fraction of frozen liver tissue from adult male and female ICR/CD1 mice that were treated with a TCPOBOP delivered using either a Low Corn Oil vehice or a High Corn Oil vehicle regimen. Livers were collected and nuclear RNA purified and analyzed either 2 week or 8 weeks after initiating TCPOBOP treatment. These samples are part of a study designed to elucidate genes and gene-based mechanisms underlying TCPOBOP-disrupted liver metabolic dysfunction, including the pericentral steatosis seen within 2 weeks of the initial TCPOBOP exposure. Major findings of this work included the following: Early (1-day) TCPOBOP transcriptional responses were enriched for CAR-bound primary response genes, and for lipogenesis and xenobiotic metabolism and oxidative stress protection pathways; late (2-wk) TCPOBOP responses included many CAR binding-independent secondary response genes, with enrichment for macrophage activation, immune response and cytokine and reactive oxygen species production. Late upstream regulators specific to TCPOBOP-exposed male liver were linked to pro-inflammatory responses and hepatocellular carcinoma progression. TCPOBOP administered weekly to male mice using a high corn oil vehicle activated carbohydrate-responsive transcription factor (MLXIPL)-regulated target genes, dysregulated mitochondrial respiratory and translation regulatory pathways, and induced more advanced liver pathology. Overall, TCPOBOP exposure recapitulated histological and gene expression changes characteristic of emerging steatotic liver disease, including secondary gene responses in liver non-parenchymal cells indicative of transition to a more advanced disease state.
2024-04-07 | GSE248858 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE13688: Effect of TCPOBOP and PCN in combination with high-cholesterol diet on genes involved in cholesterol homeostasis GSE13689: Effect of rosuvastatin and atorvastatin in combination with high-cholesterol diet on cholesterol homeostasis Refer to individual Series
2010-10-08 | E-GEOD-13721 | biostudies-arrayexpress
Project description:This work is part of a larger study where we investigated activation of the nuclear receptor and transcription factor CAR (Nr1i3) by its specific agonist ligand TCPOBOP (1,4-bis[2-(3,5-dichloropyridyloxy)]benzene), which dysregulates hundreds of genes in mouse liver and is linked to male-biased hepatocarcinogenesis. We used DNase-seq and DNase hypersensitivity site (DHS) analysis to identify several thousand genomic regions (∆DHS) where short-term exposure to TCPOBOP induces localized changes (increases or decreases) in mouse liver chromatin accessibility, many of which cluster together with TCPOBOP-responsive genes. Sites of chromatin opening were highly enriched nearby genes induced by TCPOBOP and chromatin closing was highly enriched nearby genes repressed by TCPOBOP, consistent with TCPOBOP-responsive ∆DHS serving as enhancers and promoters that positively regulate CAR-responsive genes. Gene expression changes lagged behind chromatin opening or closing for a subset of TCPOBOP-responsive ∆DHS. DHS that were specifically responsive to TCPOBOP in male liver were significantly enriched for genomic regions with a basal male bias in chromatin accessibility; however, the male-biased response of hepatocellular carcinoma-related genes to TCPOBOP was not associated with a correspondingly male-biased ∆DHS response. These studies elucidate the genome-wide organization of CAR-responsive genes and of the thousands of associated genomic sites where TCPOBOP exposure induces both rapid and persistent changes in chromatin accessibility.
2018-04-09 | GSE104061 | GEO
Project description:Changes in the activating histone-H3 chromatin marks K4me1, K4me3, and K27ac were assayed in male mouse liver following exposure to TCPOBOP, an agonist ligand of the nuclear receptor CAR (constitutive androstane receptor). This work is part of a larger study, entitled: "Widespread Epigenetic Changes to the Enhancer Landscape of Mouse Liver Induced by a Specific Xenobiotic Agonist Ligand of the Nuclear Receptor CAR" (Tox Sci, 2019).
2020-04-28 | GSE104060 | GEO