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Chromatin immunoprecipitation (ChIP) of aryl hydrocarbon receptor (AHR) in mouse colon stem cells

ABSTRACT: Chromatin immunoprecipitation (ChIP) of aryl hydrocarbon receptor (AHR) in mouse colon stem cells

PROVIDER: PRJNA743917 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15044504.fastq.gz	Fastqsanger.gz
	SRR15044505.fastq.gz	Fastqsanger.gz
	SRR15044506.fastq.gz	Fastqsanger.gz
	SRR15044507.fastq.gz	Fastqsanger.gz
	SRR15044508.fastq.gz	Fastqsanger.gz

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Chromatin immunoprecipitation (ChIP) of aryl hydrocarbon receptor (AHR) in mouse colon stem cells

Project description:To identify direct targets of the environmental sensor AHR, a nuclear transcription factor, in the colonic stem cells, we have performed ChIP sequencing of AHR bound DNA in wildtype colon organoids. ChIP sequencing of AHR knockout organoids was used as a control to filter out non-specific antibody targets.

2022-02-09 | GSE179479 | GEO

Effect of aryl hydrocarbon receptor (Ahr) gene knockout on expression profiles of murine hematopoietic stem cells

Project description:As part of a study of the role of the aryl hydrocarbon receptor (Ahr) in maintenance and senescence of hematopoietic stem cells (HSC), global gene expression profiling was done with HSC isolated from Ahr-knockout and wild-type mice. HSC from young-adult (8 wk old) AhR-KO mice had changes in expression of many genes related to HSC maintenance, consistent with the phenotype observed in aging Ahr-KO mice: decreased survival rate, splenomegaly, increased circulating white blood cells, hematopoietic cell accumulation in tissues, anemia, increased numbers of stem/progenitor and lineage-committed cells in bone marrow, decreased erythroid progenitor cells in bone marrow, and decreased self-renewal capacity of HSC. 7 samples: 3 Ahr knockout, 4 wild-type

2013-11-08 | E-GEOD-46976 | biostudies-arrayexpress

Effect of aryl hydrocarbon receptor (Ahr) gene knockout on expression profiles of aged (18-month-old) murine hematopoietic stem cells

Project description:As part of a study of the role of the aryl hydrocarbon receptor (Ahr) in maintenance and senescence of hematopoietic stem cells (HSC), global gene expression profiling was done with HSC isolated from 18-month-old Ahr-knockout and wild-type mice. HSC from aged AhR-KO mice had changes in expression of many genes related to HSC maintenance, consistent with the phenotype observed in aging Ahr-KO mice: decreased survival rate, splenomegaly, increased circulating white blood cells, hematopoietic cell accumulation in tissues, anemia, increased numbers of stem/progenitor and lineage-committed cells in bone marrow, decreased erythroid progenitor cells in bone marrow, and decreased self-renewal capacity of HSC. 10 samples: 5 Ahr knockout, 5 wild-type

2015-03-28 | E-GEOD-67378 | biostudies-arrayexpress

Transcriptome profiles of colonic stem cells of WT and AHR deficient mice treated with either DMSO or high affinity AHR ligand, FICZ for 4 hours

Project description:To identify aryl hydrocarbon receptor (AHR) dependent transcriptional changes in mouse colon stem cells, we performed RNA sequencing of colon organoids from wildtype and AhR deficient mice stimulated with an high affinity AHR ligand, 5nM FICZ for 4 hours.

2022-02-09 | GSE179481 | GEO

Effect of aryl hydrocarbon receptor (Ahr) gene knockout on expression profiles of murine hematopoietic stem cells

2013-11-08 | GSE46976 | GEO

Aryl hydrocarbon receptor (AHR)-dependent protection against lung vascular leakage in viral infection

Project description:Disruption of the lung endothelial-epithelial cell barrier during respiratory virus infection causes cell and fluid accumulation in the air spaces and compromises vital gas exchange function. Endothelial cell dysfunction is known to exacerbate tissue damage; however, it is unclear whether the lung endothelium engages in tissue-protective activity during viral infection. Here we show that the environmental sensor aryl hydrocarbon receptor (AHR) is predominantly active in endothelial cells and protects against influenza-induced lung damage. Endothelial-specific AHR deletion caused increased vascular leakage in air spaces and enhanced influenza-induced lung tissue pathology. Global expression profiling revealed limited AHR-dependent regulation of vessels in the steady-state lung. However, following influenza-induced tissue damage and inflammation, AHR engages tissue-protective programmes in endothelia and prevents a dysplastic keratinised and apoptotic signature in the airways of infected lungs.

2023-05-23 | GSE203427 | GEO

Chromatin Immunoprecipitation Analysis of Aryl Hydrocarbon Receptor Binding in a Mouse B-cell Line (CH12.LX) Activated with Lipopolysaccharide and Treated with 2,3,7,8-Tetrachlorodibenzo-p-dioxin

Project description:The aryl hydrocarbon receptor (AHR) agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) alters differentiation of B cells and suppresses antibody production. The objectives of this study was to use a combination of whole genome, microarray-based chromatin immunoprecipitation (ChIP-on-chip) and time course gene expression microarray analysis on the mouse B-cell line CH12.LX following exposure to lipopolysaccharide (LPS) or LPS and TCDD to identify the primary and downstream transcriptional elements of B-cell differentiation that are altered by the AHR.

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Effect of bone marrow-specific aryl hydrocarbon receptor (Ahr) gene knockout on expression profiles of hematopoietic stem cells from young and old mice.

Project description:As part of a study of the role of the aryl hydrocarbon receptor (Ahr) in maintenance and senescence of hematopoietic stem cells (HSC), global gene expression profiling was done with HSC isolated from bone marrow restricted conditional Ahr-knockout and AhR floxed mice. HSC from young-adult (8 wk old) cAhR-KO mice had changes in expression of many genes related to HSC maintenance, consistent with the phenotype observed in Ahr-KO mice. Aged cAhR-KO mice (18 months old) also displayed alterations in peripheral white blood cell counts, serial repopulation potential and levels of ROS in bone marrow cells, consistent with previous observations on the role of AhR in the hematopoietic system. 22 samples: 5 young Ahr knockout, 6 old Ahr knockout, 5 young floxed Ahr, 6 old floxed Ahr

2016-06-30 | E-GEOD-76276 | biostudies-arrayexpress

The Aryl hydrocarbon receptor and FOS mediated cytotoxicity induced by Acenatobacter baumannii

Project description:Acinetobacter baumannii is a highly pathogenic and multidrug-resistant Gram-negative bacterium that causes severe nosocomial infections. To better understand the mechanism of pathogenesis, we compare the proteomes of uninfected and infected human cells, revealing that transcription factor FOS is the host protein most strongly induced by A. baumannii infection. Pharmacological inhibition of FOS reduces the cytotoxicity of A. baumannii in cell-based models, and similar results are also observed in a mouse infection model. A. baumannii outer membrane vesicles (OMVs) are shown to activate the aryl hydrocarbon receptor (AHR) of host cells by inducing the host enzyme tryptophan-2,3-dioxygenase (TDO), producing the ligand kynurenine, which binds AHR. Following ligand binding, AHR is a direct transcriptional activator of the FOS gene. Our results suggest that bacterial infection interacts with host tryptophan metabolism and the transcription factor FOS.

2024-08-05 | PXD053768 | Pride

Expression data of primary melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice

Project description:[original Title] Comparison of expression data of primary murine melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice Melanin is produced exclusively by melanocytes and melanogenesis is the vital response to protect skin cells against Ultraviolet B (UVB)-induced DNA damage. The aryl hydrocarbon receptor (AhR) is a transcription factor, which may be involved in the physiological tanning response. Normal murine melanocytes express functional AhR. We tested gene expression in WT versus AhR-deficient mice primary murine melanocytes, isolated from the skin and cultivated for several passages. Skin epidermal cells from 2 individual C57BL/6 mice and 2 individual AhR-deficient mice (deletion of exon2, AhRtm1Bra) were grown for 6-8 weeks in selection medium to propagate melanocytes.

2010-09-05 | E-GEOD-19411 | biostudies-arrayexpress

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