Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18163557.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 1 of 1 |
Similar Datasets
Project description:NADPH-cytochrome P450 reductase (CPR) is important for the functions of many enzymes, such as microsomal cytochrome P450 (P450) monooxygenases and heme oxygenases. Two mouse models with deficient CPR expression in adults were recently generated in this laboratory: liver-Cpr-null (with liver-specific Cpr deletion) (Gu et al., J. Biol. Chem., 278, 25895–25901, 2003) and Cpr-low (with reduced CPR expression in all organs examined) (Wu et al. J. Pharmacol. Expt. Ther. 312, 35-43, 2005). The phenotypes included a reduced serum cholesterol level and an induction of hepatic P450 in both models, and hepatomegaly and fatty liver in the liver-Cpr-null mouse alone. Our aim was to identify hepatic gene-expression changes related to these phenotypes. Cpr-lox mice, which have normal CPR expression (Wu et al., Genesis, 36, 177-181, 2003.), were used as the control in microarray analysis. A detailed analysis of the gene-expression changes in lipid metabolism and transport pathways revealed potential mechanisms, such as an increased activation of constitutive androstane receptor (CAR) and a decreased activation of peroxisomal proliferators activated receptor alpha (PPAR-gamma) by precursors of cholesterol biosynthesis, that underlie common changes (e.g., induction of multiple P450s and inhibition of genes for fatty acids metabolism) in response to CPR-loss in the two mouse models. Moreover, we also uncovered model-specific gene-expression changes, such as the induction of a lipid translocase (CD36 antigen) and the suppression of carnitine O-palmitoyltransferase 1 (CPT1a) and acyl-CoA synthetase long-chain family member 1 (Acsl1), that are potentially responsible for the severe hepatic lipidosis observed in liver-Cpr-null, but not Cpr-low mice. Keywords = Cytochrome P450 Keywords = NADPH-cytochrome P450 reductase Keywords = transgenic mice Keywords = liver Keywords = nuclear receptor Keywords: other
2005-07-16 | GSE2362 | GEO
Project description:The NADPH-cytochrome P450 reductase (CPR) is essential for the functioning of microsomal cytochrome P450 (P450) monoxygenases. The biological functions of the CPR-dependent enzymes in the intestine are not known, despite the vast knowledge available on the biochemical properties of the various oxygenases. A mouse model with intestinal epithelium (IE)-specific Cpr-knockout (IE-Cpr-null) was recently generated in this laboratory (Zhang et al., Drug Metab. Dispos., 37, 651-657, 2009). The IE-Cpr-null mice did not display any obvious abnormalities in growth, development, or reproduction, and their intestines appeared to have a normal structure. Despite the absence of observable phenotypes, we hypothesized that loss of the enterocyte CPR expression will impact homeostasis of endogenous compounds, and expression of genes, that have critical biological function in the small intestine. In the present study, we have performed genomic analyses for enterocytes from IE-Cpr-null mice and their wild-type littermates, using Affymetrix Mouse Expression Set 430A 2.0 GeneChip Arrays. Our aim was to identify small intestinal gene-expression changes, which may shed light on potential biological roles of CPR and CPR-dependent enzymes in the small intestine. Our analysis revealed significant expression increases in P450s, transporters, cholesterol biosynthesis, and (unexpectedly) antigen presentation/processing. Further genomic and biochemical analyses revealed potential mechanisms linking CPR-dependent enzymes and the expression of major histocompatibility complex class II genes in the small intestine.
2012-04-11 | GSE35293 | GEO
Project description:NADPH-cytochrome P450 reductase (CPR) is important for the functions of many enzymes, such as microsomal cytochrome P450 (P450) monooxygenases and heme oxygenases. Two mouse models with deficient CPR expression in adults were recently generated in this laboratory: liver-Cpr-null (with liver-specific Cpr deletion) (Gu et al., J. Biol. Chem., 278, 25895-25901, 2003) and Cpr-low (with reduced CPR expression in all organs examined) (Wu et al. J. Pharmacol. Expt. Ther. 312, 35-43, 2005). The phenotypes included a reduced serum cholesterol level and an induction of hepatic P450 in both models, and hepatomegaly and fatty liver in the liver-Cpr-null mouse alone. Our aim was to identify hepatic gene-expression changes related to these phenotypes. Cpr-lox mice, which have normal CPR expression (Wu et al., Genesis, 36, 177-181, 2003.), were used as the control in microarray analysis. A detailed analysis of the gene-expression changes in lipid metabolism and transport pathways revealed potential mechanisms, such as an increased activation of constitutive androstane receptor (CAR) and a decreased activation of peroxisomal proliferators activated receptor alpha (PPARï?¡) by precursors of cholesterol biosynthesis, that underlie common changes (e.g., induction of multiple P450s and inhibition of genes for fatty acids metabolism) in response to CPR-loss in the two mouse models. Moreover, we also uncovered model-specific gene-expression changes, such as the induction of a lipid translocase (CD36 antigen) and the suppression of carnitine O-palmitoyltransferase 1 (CPT1a) and acyl-CoA synthetase long-chain family member 1 (Acsl1), that are potentially responsible for the severe hepatic lipidosis observed in liver-Cpr-null, but not Cpr-low mice.
2007-08-31 | E-GEOD-2362 | biostudies-arrayexpress
Project description:Virus infection and over expression of protein in cytosol induce a subset of HSP70s. We named this response the Cytosolic Protein Response (CPR) and have been investigating it in the context of a parallel mechanism in the soluble cytosol with the UPR, and as a subcomponent of the larger HS response. This experiment was carried out to study the transcriptional aspect of CPR. In this analysis, we have triggered CPR by infiltrating proline analogue, L-azetidine-2-carboxylic acid (AZC) into Arabidopsis mature leaves. Since AZC trigger unfolded protein response(UPR) in ER as well as CPR, we have included tunicamycin treatment, which is a specific inducer of UPR to subtract the effect of UPR from the AZC response. Heat shocked samples were included to identify CPR as a subcomponent of larger HS response. We used microarray data to identify the genes upregurated by CPR. These genes were commonly upregulated by AZC and HS but not by tunicamycin treatment. Keywords: stress response
2008-12-11 | GSE11758 | GEO
Project description:The NADPH-cytochrome P450 reductase (CPR) is essential for the functioning of microsomal cytochrome P450 (P450) monoxygenases. The biological functions of the CPR-dependent enzymes in the intestine are not known, despite the vast knowledge available on the biochemical properties of the various oxygenases. A mouse model with intestinal epithelium (IE)-specific Cpr-knockout (IE-Cpr-null) was recently generated in this laboratory (Zhang et al., Drug Metab. Dispos., 37, 651-657, 2009). The IE-Cpr-null mice did not display any obvious abnormalities in growth, development, or reproduction, and their intestines appeared to have a normal structure. Despite the absence of observable phenotypes, we hypothesized that loss of the enterocyte CPR expression will impact homeostasis of endogenous compounds, and expression of genes, that have critical biological function in the small intestine. In the present study, we have performed genomic analyses for enterocytes from IE-Cpr-null mice and their wild-type littermates, using Affymetrix Mouse Expression Set 430A 2.0 GeneChip Arrays. Our aim was to identify small intestinal gene-expression changes, which may shed light on potential biological roles of CPR and CPR-dependent enzymes in the small intestine. Our analysis revealed significant expression increases in P450s, transporters, cholesterol biosynthesis, and (unexpectedly) antigen presentation/processing. Further genomic and biochemical analyses revealed potential mechanisms linking CPR-dependent enzymes and the expression of major histocompatibility complex class II genes in the small intestine. Adult (2.5-3.0 month-old) male IE-Cpr-null and WT litermates were used for all experiments. RNA was collected from eight mice of each genotype and RNA from two mice of the same genotype was pooled prior to hybridization to the microarray to create a total of four samples for each genotype.
2012-04-10 | E-GEOD-35293 | biostudies-arrayexpress
Project description:Grapevines cv Sauvignon Blanc were subjected to different stress regimes by simulating the most common extreme weather events occurring within the current climate change scenario. During spring, just before bud break, the vines were either flooded or kept under normal conditions. Both vines were then split in two groups and put in differnt tunnels, either undergoing a simulated heatwave or not. Berry samples were collected from the four groups of plants (control, only flooded, only heatwave, flooded + heatwave) at different timepoints before, during and after the stress. Transcriptomic analyses were carried out on these samples along with some metabolomic assessments to characterize the response to stress in the different samples and the effect of the combined stresses.
2023-01-06 | GSE206753 | GEO
Project description:Virus infection and over expression of protein in cytosol induce a subset of HSP70s. We named this response the Cytosolic Protein Response (CPR) and have been investigating it in the context of a parallel mechanism in the soluble cytosol with the UPR, and as a subcomponent of the larger HS response. This experiment was carried out to study the transcriptional aspect of CPR. In this analysis, we have triggered CPR by infiltrating proline analogue, L-azetidine-2-carboxylic acid (AZC) into Arabidopsis mature leaves. Since AZC trigger unfolded protein response(UPR) in ER as well as CPR, we have included tunicamycin treatment, which is a specific inducer of UPR to subtract the effect of UPR from the AZC response. Heat shocked samples were included to identify CPR as a subcomponent of larger HS response. We used microarray data to identify the genes upregurated by CPR. These genes were commonly upregulated by AZC and HS but not by tunicamycin treatment. Experiment Overall Design: Arabidopsis mature leaves were infiltrated with AZC or L-Proline (control of AZC) and tunicamycin or DMF(solvent control of tunicamycin). For the heat shock treatment, six mature leaves were detached from plant and incubated at 37 °C or 20°C (as a control) for a period of 1h. The experiment was repeated three times for AZC and HS treatment (3 biological replication). Tunicamycin experiment was repeated five times due to large valiation in the responses (5 biological replication).
2009-01-13 | E-GEOD-11758 | biostudies-arrayexpress
Project description:Altered hepatic gene expression in liver-Cpr-null and Cpr-low mice
| PRJNA91211 | ENA
Project description:Microarray analysis to examine the relationship between hepatic phenotype and changes in gene expression in cytochrome P450 reductase (CPR) null mice. Keywords: ordered
2004-07-11 | GSE1468 | GEO