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Transcriptional impact of EGFR-AT1R-crosstalk (Stable transfection of AT1R in HEK293 cells)

ABSTRACT: The impact of AT1R and EGFR on SRF transcriptional activity, signaling pathways and transcriptome regulation were investigated in HEK293, HK-2 and vascular smooth muscle cells, applying reporter gene, protein and mRNA expression techniques as well as RNAseq followed by bioinfor-matic analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE162768 | GEO | 2022/01/10

REPOSITORIES: GEO

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Transcriptional impact of EGFR-AT1R-crosstalk (Transient transfection of AT1R in HEK293 cells)

Project description:The impact of AT1R and EGFR on SRF transcriptional activity, signaling pathways and transcriptome regulation were investigated in HEK293, HK-2 and vascular smooth muscle cells, applying reporter gene, protein and mRNA expression techniques as well as RNAseq followed by bioinfor-matic analysis.

2022-01-10 | GSE162769 | GEO

Transcriptional impact of EGFR-AT1R-crosstalk (Stable transfection of AT1R in HEK293 cells)

Project description:Transcriptional impact of EGFR-AT1R-crosstalk (Stable transfection of AT1R in HEK293 cells)

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Transcriptional impact of EGFR-AT1R-crosstalk (Transient transfection of AT1R in HEK293 cells)

Project description:Transcriptional impact of EGFR-AT1R-crosstalk (Transient transfection of AT1R in HEK293 cells)

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Transcriptional impact of EGFR-AT1R-crosstalk

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Transcriptional impact of EGFR-AT1R-TP receptor crosstalk in mouse aortic vascular smooth muscle cells

Project description:The impact EGFR, AT1R and TP receptor individual or simultaneous activations on the gene expression was investigated in mouse aortic vascular smooth muscle cells (aVSMC)

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Transcriptional impact of EGFR-AT1R-crosstalk

Project description:This SuperSeries is composed of the SubSeries listed below.

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EWS-FLI1-transfection of HEK293

Project description:Response of HEK293-cells after transfection with EWS-FLI1. HEK293 cells were transfected with the expression vector pIRES2-EGFP containing type I EWS-FLI1 or empty control vector. For transient transfection standard DEAE dextran method was used and RNA was isolated 48h post transfection. For stable transfection cells were transfected using FuGENE 6 (Roche, Mannheim, Germany) and cells were selected with 400 ug/mL G418. DNA-microarray analysis was performed using Affymetrix HG-U133A microarrays.(see Staege et al. Cancer Res. 2004) Keywords = HEK293 Keywords = EWS-FLI1 Keywords = Ewing family tumors Keywords: other

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Transcriptional impact of EGFR-AT1R-TP receptor crosstalk in mouse aortic vascular smooth muscle cells

Project description:Transcriptional impact of EGFR-AT1R-TP receptor crosstalk in mouse aortic vascular smooth muscle cells

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Mapping AT1R biased signaling using proximity-labeling and proteomics identifies diverse actions of biased agonists

Project description:Angiotensin II type 1 receptors (AT1Rs) are one of the most widely studied G protein-coupled receptors. To fully appreciate the diversity in cellular signaling profiles activated by AT1R transducer-biased ligands, we utilized peroxidase-catalyzed proximity labeling to capture proteins in close proximity to AT1Rs in response to six different ligands: Angiotensin II (full agonist), S1I8 (partial agonist), TRV055 and TRV056 (G protein-biased agonists), TRV026 and TRV027 (β-arrestin biased agonists) at 90s, 10min, and 60min after stimulation. We systematically analyzed the kinetics of AT1R trafficking and determined that distinct ligands lead AT1R to different cellular compartments for downstream signaling activation and receptor degradation/recycling. Distinct proximity labelling of proteins from a number of functional classes, including GTPases, adaptor proteins, and kinases were activated by different ligands suggesting unique signaling and physiological roles of the AT1R. Ligands within the same class, i.e. either G protein-biased or -arrestin-biased, shared high similarity in their labelling profiles. Comparison between ligand classes revealed distinct signaling activation such as greater labeling by G protein biased ligands on ESCRT-0 complex proteins that act as sorting machinery for ubiquitinated proteins. Our study provides a comprehensive analysis of AT1R receptor trafficking kinetics and signaling activation profiles induced by distinct classes of ligands.

2021-03-25 | PXD023814 | Pride

Role of redox-dependent, flow-related regulation of AT1R expression in collateral growth impairment

Project description:Genomic analysis of control and collateral arteries was used to investigate mechanisms responsible for impaired collateral growth in the Spontaneously Hypertensive rat, an animal model of essential hypertension with increased oxidative and nitrosative stress and metabolic abnormalities. A fundamental difference was observed in the overall expression pattern in SHR vs WKY collaterals. Redox related genes with altered expression included cyba (the gene encoding p22phox), superoxide dismutase 3, and thioredoxin reductases 1 and 2. Cystatin C, hevin, angiotensinogen, and the angiotensin type 1b receptor (AT1bR) had altered collateral expression that was confirmed by RT-PCR. These molecules are known to have significant roles in other types of arterial remodeling. Of specific interest was the AT1bR which exhibited up-regulation in WKY collaterals, but down-regulation in SHR. A remarkable increase in AT1R protein was observed in WKY but not SHR collaterals. Pharmacological blockade of the AT1R with losartan prevented collateral luminal expansion in WKY. In SHR, captopril restored redox status assessed by cyba expression and nitric oxide concentration, prevented collateral AT1bR down-regulation and re-established the capacity for collateral growth. These results indicate that redox-status significantly alters flow-mediated transcriptional regulation and demonstrate that increased flow-related expression/activation of the AT1R is required for normal collateral luminal expansion but is altered by chronic oxidative and/or nitrosative stress in hypertensive rats. Keywords: gene expression two strains: two vessel types

2010-12-15 | E-GEOD-19524 | biostudies-arrayexpress

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