Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Arylhydrocarbon receptor and the cytochrome P450 enzyme CYP1B1 prevent exacerbation of allergic airway inflammation

ABSTRACT: Arylhydrocarbon receptor and the cytochrome P450 enzyme CYP1B1 prevent exacerbation of allergic airway inflammation

PROVIDER: PRJNA666336 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12739206.fastq.gz	Fastqsanger.gz
	SRR12739207.fastq.gz	Fastqsanger.gz
	SRR12739208.fastq.gz	Fastqsanger.gz
	SRR12739209.fastq.gz	Fastqsanger.gz
	SRR12739210.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 31

Similar Datasets

Arylhydrocarbon receptor and the cytochrome P450 enzyme CYP1B1 prevent exacerbation of allergic airway inflammation

Project description:Signaling via the arylhydrocarbon receptor (AhR) is thought to contribute to exacerbation of allergic asthma by anthropogenic pollution. The physiological role of AhR and its downstream targets CYP1 family members upon exposure to aeroallergens remain unknown. We seek to characterize the role of the AhR pathway for the regulation of allergic airway inflammation (AAI). We employed knockout animals of the AhR and its downstream target cytochrome P450 enzymes CYP1A1, CYP1A2 and CYP1B1 and subjected them to preclinical allergic asthma models (ragweed and house dust mite) to assess the role of AhR and CYP1 family members in allergic airway inflammation. Histological, transcriptional and functional assays were used to uncover relevant cell types and mechanistic insights. In the ragweed model, AhRKO/KO and CYP1B1KO/KO but not CYP1A2 KO/KO or CYP1A2KO/KO animals showed exacerbation of AAI including elevated infiltration of cells in the bronchoalveolar lavage fluid and increased serum levels of IgE and allergen-specific IgG1. AhR KO/KO and CYP1B1KO/KO animals showed also more severe reactions in HDM-induced allergic AAI. Bone marrow chimeras as well as qPCR analysis and immune fluorescence histology indicate that expression of CYP1B1 in non-hematopoietic cells – presumably lung epithelial cells – is necessary to prevent exacerbation of HDM-induced AAI. Mechanistically, we show that CYP1B1 deficiency leads to enhanced expression and activity of CYP1A1 in lung epithelial cells and thus potentially to deprivation from endogenous AhR ligands. Transcriptional analysis of primary lung epithelial cells indicates a functional link of the AhR to regulation of circadian clock genes at baseline and massive alteration of gene expression upon allergen exposure.

2022-05-23 | GSE158715 | GEO

Identification and developmental expression of the full complement of cytochrome P450 genes in zebrafish

Project description:To determine the expression of cytochrome P450 genes during normal development

2010-10-21 | GSE24840 | GEO

Identification and developmental expression of the full complement of cytochrome P450 genes in zebrafish

Project description:To determine the expression of cytochrome P450 genes during normal development Zebrafish embryos were collected at 3, 6, 12, 24, 36, and 48 hours post fertilization. Quadruplicate biological replicates of 100 embryos were hybridized.

2010-10-21 | E-GEOD-24840 | biostudies-arrayexpress

Fetal to adult ontogeny of human cytochrome P450 activity, abundance, and expression

Project description:Activity-based and global proteomic analysis of fetal through late adulthood human samples, with a primary focus on cytochrome P450 enzyme expression and functional activity

2018-10-24 | PXD002781 | Pride

Endothelial deletion of the cytochrome P450 reductase leads to cardiac remodelling

Project description:Endothelial deletion of the cytochrome P450 reductase leads to cardiac remodelling

| PRJNA887058 | ENA

Identification of genes responding to the activity of the Arabidopsis cytochrome P450 KLUH/CYP78A5

Project description:The Arabidopsis cytochrome P450 KLUH (KLU)/CYP78A5 promotes organ growth in a non-cell autonomous manner. To identify genes regulated by KLU activity, homozygous klu-2 mutants carrying constructs for EtOH-inducible overexpression of wild-type KLU (35S::AlcR-AlcA::KLU) or of enzymatically inactive KLU protein (35S::AlcR-AlcA::KLUmut) were induced with EtOH and sampled at 90 min and 240 min after induction for gene expression changes. Keywords: Time course, genetic modification

2007-12-04 | GSE9201 | GEO

Transcription profiling of mouse models with liver-specific deletion or global hypomorphic expression of the NADPH-cytochrome P450 reductase gene to study molecular mechanisms for the regulation of microsomal cytochrome P450 and the fatty liver phenotype.

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

Endothelial deletion of the cytochrome P450 reductase leads to cardiac remodelling

Project description:The cytochrome P450 reductase (POR) transfers electrons to all microsomal cytochrome P450 enzymes (CYP450) thereby driving their activity. In the vascular system, the POR/CYP450 system has been linked to the production of epoxyeicosatrienoic acids (EETs) but also to the generation of reactive oxygen species. In cardiac myocytes (CMs), EETs have been shown to modulate the cardiac function and have cardioprotective effects. The functional importance of the endothelial POR/CYP450 system in the heart is unclear and was studied here using endothelial cell-specific, inducible knockout mice of POR (ecPOR-/-). RNA sequencing of murine cardiac cells revealed a cell type-specific expression of different CYP450 homologues. Cardiac endothelial cells mainly expressed members of the CYP2 family which produces EETs, and of the CYP4 family that generates omega fatty acids. Tamoxifen-induced endothelial deletion of POR in mice led to cardiac remodelling under basal conditions, as shown by an increase in heart weight to body weight ratio and an increased CM area as compared to control animals. Endothelial deletion of POR was associated with a significant increase in endothelial genes linked to protein synthesis with no changes in genes of the oxidative stress response. CM of ecPOR-/- mice exhibited attenuated expression of genes linked to mitochondrial function and an increase in genes related to cardiac myocyte contractility. In a model of pressure overload (transverse aortic constriction, TAC with O-rings), ecPOR-/- mice exhibited an accelerated reduction in cardiac output (CO) and stroke volume (SV) as compared to control mice. These results suggest that loss of endothelial POR along with a reduction in EETs leads to an increase in vascular stiffness and loss in cardioprotection, resulting in cardiac remodelling.

2022-12-21 | GSE214776 | GEO

Cytochrome P450 Monooxygenase Mediated Metabolic Utilization of Benzo(a)pyrene by Fungi

Project description:Cytochrome P450 Monooxygenase Mediated Metabolic Utilization of Benzo(a)pyrene by Fungi

| PRJNA480272 | ENA

Developmental effects of maternal dietary vitamin A deficiency and P450 cytochrome 1b1 deletion in mice

Project description:Wild type C57Bl/6J, Cyp1b1-null, and a substrain of Cyp1b1-null that are resistant to diet-induced obesity (Resistant Cyp1b1-null) timed mated pregnant dams were administered either a defined vitamin A sufficient diet or matched vitamin A deficient diet from embryonic day 4.5. Offspring liver gene expression was examined at birth (post-natal day 0) and at weaning (post-natal day 21).

2016-10-12 | GSE87844 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data