Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA283858 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptomic profiling of liver of Ctnnb1-KO and WT mice after 12 weeks exposure to Phenobarbital (miRNA)
| PRJNA283853 | ENA
Project description:Signaling through the Wnt/b-catenin pathway is a crucial determinant of hepatic zonal gene expression, liver development, regeneration, and tumorigenesis. The gene encoding b-catenin is called Ctnnb1. We have previously shown, that liver tumour promotion mediated by the model tumour promoter phenobarbital (PB) is completely lost in mice, where Ctnnb1 has been conditionally knocked out in hepatocytes (CTNNB1KO mice; Rignall et al., Carcinogenesis 32, 52-57, 2010). In the present study, the effect of a 12 weeks PB exposure on the liver miRNA expression pattern was investigated, in order to potentially get information on the nature of the loss of promotional activity in the CTNNB1KO mice.
2018-05-11 | GSE68779 | GEO
Project description:Signaling through the Wnt/b-catenin pathway is a crucial determinant of hepatic zonal gene expression, liver development, regeneration, and tumorigenesis. The gene encoding b-catenin is called Ctnnb1. We have previously shown that liver tumour promotion mediated by the model tumour promoter phenobarbital (PB) is completely lost in mice, where Ctnnb1 has been conditionally knocked out in hepatocytes (CTNNB1KO mice; Rignall et al., Carcinogenesis 32, 52-57, 2010). In the present study, the effect of a 12 weeks PB exposure on the liver miRNA expression pattern was investigated, in order to potentially get information on the nature of the loss of promotional activity in the CTNNB1KO mice.
2018-05-11 | GSE68786 | GEO
Project description:Adult (12 weeks old) WT, LKO and KO male mice from C57Bl6J were either treated with a control diet (CTRL) or an High Fat Diet (HFD) during 12 weeks prior to liver gene expression analysis
2018-12-05 | GSE123354 | GEO
Project description:Co-chaperone protein CAR Cytoplasmic Retention Protein (CCRP) interacts with various nuclear receptors and determines their localization. However, there is limited information about in vivo role of CCRP especially in nuclear receptor-mediated gene regulation. We have generated CCRP global knockout (KO) mouse and have employed whole genome microarray analysis to reveal the role of CCRP in gene regulation in the mouse liver treated with phenobarbital (CAR activator) or non-treated. Male WT and KO mice were fasted for 24 h followed by the treatment with phenobarbital or vehicle PBS for 6h. Phenobarbital significantly induced or repressed 1302 and 2744 genes in WT and KO, respectively. Interestingly, cholesterol synthesizing genes were significantly up-regulated in KO even without treatment.
2015-01-05 | GSE56557 | GEO
Project description:In rodent liver, a single injection of N-nitrosodiethylamine (DEN) followed by chronic treatment with the antiepileptic drug phenobarbital (PB) promotes the outgrowth of hepatocellular tumors with activating mutations in Ctnnb1, encoding the transcription factor β-catenin. We now studied long-term effects of PB treatment in livers of transgenic mice with hepatocyte-specific knockout (KO) of Apc, a negative regulator of β-catenin signaling. The number of Apc KO hepatocytes present in the liver decreased with age, indicative of a selective disadvantage of Apc KO cells in the absence of PB. Following liver tumor promotion by PB in Apc KO mice for 9 months, tumor burden was quantified and histological appearance, gene expression profiles, and activity of oncogenic signaling pathways of the tumors were analyzed. In Apc KO mice fed with PB, we observed an increased hepatic tumor volume fraction and tumor multiplicity, as compared to non-promoted animals. Tumors in the PB-treated Apc KO group were mostly eosinophilic hepatocellular adenoma with activated β-catenin, due to the deletion of Apc. These tumors exhibited striking phenotypic similarities to DEN-induced Ctnnb1-mutated tumors, regarding histological appearance and expression of marker proteins and mRNAs. A particular sub-population of tumors, Apc KO-driven basophilic hepatocellular carcinomas, exclusively appeared in the non-PB-treated group but was absent from PB-promoted livers. In conclusion, phenobarbital promotes the outgrowth of Apc-deficient, β-catenin-activated hepatocellular adenoma while simultaneously inhibiting the formation of a certain population of Apc-driven hepatocellular carcinoma.
2018-05-17 | GSE68969 | GEO
Project description:mRNA expression profiles from interscapular brown adipose (iBAT) tissue male ATF4 BAT KO mice and their WT counterparts after 12 weeks of high fat diet.
2025-07-28 | GSE291759 | GEO
Project description:Co-chaperone protein CAR Cytoplasmic Retention Protein (CCRP) interacts with various nuclear receptors and determines their localization. However, there is limited information about in vivo role of CCRP especially in nuclear receptor-mediated gene regulation. We have generated CCRP global knockout (KO) mouse and have employed whole genome microarray analysis to reveal the role of CCRP in gene regulation in the mouse liver treated with phenobarbital (CAR activator) or non-treated. Male WT and KO mice were fasted for 24 h followed by the treatment with phenobarbital or vehicle PBS for 6h. Phenobarbital significantly induced or repressed 1302 and 2744 genes in WT and KO, respectively. Interestingly, cholesterol synthesizing genes were significantly up-regulated in KO even without treatment. Mice were fasted for 24 h followed by the intraperitoneally treatment with PBS or phenobarbital at dose of 100 mg/kg body weight for 6 h, or non-treatment.
2015-01-05 | E-GEOD-56557 | biostudies-arrayexpress
Project description:Identification of beta-catenin interacting proteins via affinity purification with anti-beta-catenin antibody or IgG control in WT (NTC control) or Ikzf1/Ikzf3-KO (dual CRISPR KO) BCR-ABL1 transformed murine pre-B cells with CTNNB1 activation via a Ctnnb1 Ex3 fl/fl + Ert2Cre model.
2025-08-13 | PXD067318 | Pride
Project description:Lung gene expression after long-term (26 weeks, 52 weeks, 78 weeks & 104 weeks) styrene inhalation exposure at a single concentration (120ppm) in three strains of C57BL/6 mice -- wild-type (WT), CYP2F2 knockout (KO), and CYP2F1 humanized (TG) mice, and CD-1 mice. These data examine transcriptomic changes in lung tissue after long-term styrene inhalation in male C57Bl/6 and CD-1 mice. Styrene causes increased lung tumors in mice, but not in rats. Mouse lung tumors were found mostly at the conclusion of a life-time (104 weeks for males) exposure study and most were benign. Styrene is largely negative in genotoxicity assays. Styrene metabolism by CYP2F2 produced a different metabolite pattern in mouse lung than in liver or in rats or humans. The purpose of this study was to use genomic analyses to further investigate potential modes of action (MoA) of styrene in mice after long-term exposure to styrene. Mice strains exposed were C57BL/6 wild-type (WT), CYP2F2 knockout (-/-; KO) and CYP2F21 humanized transgenic (2F2-KO + 2F1,2A13,2B6-transgenic, TG), and CD-1 male mice using 120 ppm styrene at 6 hr/day 5 days/wk for 26, 52, 78 and 104 weeks. Lungs were analyzed by Affymetrix whole genome microarrays for each strain relative to sample time-specific vehicle controls for each strain.
2018-03-08 | GSE98470 | GEO