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Effect of ATM inhibition in primary endothelial cells

ABSTRACT: Effect of ATM inhibition in primary endothelial cells

PROVIDER: PRJNA589641 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10446911.fastq.gz	Fastqsanger.gz
	SRR10446912.fastq.gz	Fastqsanger.gz
	SRR10446913.fastq.gz	Fastqsanger.gz
	SRR10446914.fastq.gz	Fastqsanger.gz
	SRR10446915.fastq.gz	Fastqsanger.gz

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Effect of ATM inhibition in primary endothelial cells

Project description:Analysis of gene expresssion in HUVECs following ATM inhibition. The main objective of the study was to get insights about the metabolic pathways regulated by ATM in primary endothelial cells.Here we demonstrate that besides the DNA damage repair defect, metabolic dysregulation causes several of the phenotypes observed in AT patients. We discovered a new aspect of metabolic control by ATM, the control of cystine and arginine influx via the phosphorylation of CD98HC. Our data provide further insights into why NAC treatment and production of GSH is beneficial to AT patients aside from antioxidant effects and we propose a novel mechanistic link between these acute responses and disease manifestation.

2023-11-01 | GSE140416 | GEO

Effect of endothelial specific inhibition of Brg1

Project description:Effect of endothelial specific inhibition of Brg1

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Inhibition of ATM in Mouse-derived lung fibroblasts

Project description:The main goal is to examine the transcriptome of primary lung fibroblasts that undergo premature senescence after prolonged inhibition of ATM.

2024-12-22 | GSE182731 | GEO

Inhibition of ATM in Mouse-derived lung fibroblasts

Project description:Inhibition of ATM in Mouse-derived lung fibroblasts

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ATM inhibition enhances cancer immunotherapy by promoting mtDNA leakage/cGAS-STING activation [B16 vivo]

Project description:Novel approaches are needed to boost the efficacy of immune checkpoint blockade (ICB) therapy. Ataxia Telangiectasia Mutated (ATM) protein plays a central role in sensing DNA double strand breaks and coordinating their repair. Recent data indicated that ATM might be a promising target to enhance immune checkpoint blockade (ICB) therapy. However, the molecular mechanism involved is not clearly elucidated. Here we show that ATM inhibition could potentiate ICB therapy by promoting cytoplasmic leakage of mitochondrial DNA and activation of the cGAS/STING pathway. Genetic depletion of ATM in murine cancer cells significantly delayed tumor growth in syngeneic mouse hosts in a T-cell dependent manner. Furthermore, chemical inhibition of ATM significantly potentiated anti-PD1 therapy of mouse tumors. ATM inhibition potently activated the cGAS/STING pathway and enhanced lymphocyte infiltration into the tumor microenvironment by downregulating TFAM, which led to mitochondrial DNA leakage into the cytoplasm. Moreover, our analysis of data from a large patient cohort indicated that ATM mutations, especially nonsense mutations, predicted for clinical benefits for ICB therapy. Our study therefore provides strong evidence that ATM may serve both as a therapeutic target and a biomarker to enable ICB therapy.

2023-11-18 | GSE161922 | GEO

Effect of BMP inhibition or stimulation of primary human keratinocytes

Project description:Effect of BMP inhibition or stimulation of primary human keratinocytes

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ATM inhibition enhances cancer immunotherapy by promoting mtDNA leakage/cGAS-STING activation [4T1 in vitro]

2023-11-18 | GSE161912 | GEO

Effect of heat shock at 500 atm and pressure shock to 500 atm on Methanocaldococcus jannaschii

Project description:Growth and transcriptional profiles of the barophilic methanarchaeon Methanocaldococcus jannaschii were studied at temperatures up to 98C and pressures up to 500 atm. Application of 500 atm of hyperbaric pressure shifted the optimal growth temperature upwards, and heat shock from 88C to 98C at 500 atm resulted in termination of growth. Pressure shock of M. jannaschii from 7.8 to 500 atm over 15-min, the first pressure upshift reported for a barophile, did not accelerate growth. Transcriptional profiles indicated a similar pressure response under growth and heat shock at 500 atm and pressure shock to 500 atm suggesting that the commonly affected genes are important for high-pressure adaptation. Factorial microarray design allowed de-convolution of the interacting effect of elevated pressure and heat shock on expression profiles, thus suggesting genes that may contribute to the organism’s survival in the turbulent in situ conditions of deep-sea hydrothermal vents. Keywords: stress response, time course, high pressure, heat shock, pressure shock

2007-04-05 | GSE4620 | GEO

Axitinib exposure triggers endothelial cells senescence through ROS accumulation and ATM activation

Project description:Here we report that Axitinib, an inhibitor of VEGFRs currently in use as a second line treatment for advanced renal cell carcinoma, promotes senescence of human endothelial cells in vitro. Mechanistically, this requires oxidative stress-dependent activation of the Ataxia Telangiectasia Mutated (ATM) kinase. Induction of oxidative stress-related genes distinguishes the response of endothelial cells to Axitinib from that to doxorubicin

2019-07-02 | GSE126426 | GEO

Genome-wide mRNA expression analysis of primary cultured mouse brain microvascular endothelial cells after inhibition of PKC-beta

Project description:Pharmacological inhibition of protein kinase C beta (PKC-beta) # by the compound LY317615 has been tested on primary cultured mouse brain microvascular endothelial cells, stimulated in-vitro for 8h at a concentration of 5 ÂµM. The aim of the study was the question if inhibition of PKC-beta leads to inhibition of genes responsible for T-cell migration in order to investigate LY-317615 as a possible experimental therapy for multiple sclerosis. primary cultured mouse brain microvascular endothelial cells (MBMEC) have been prepared from new-born mice and cultured for one week. Then stimulated for 8h with 5 ÂµM LY317615. Two samples had been treated for the last 24h with 500 ÂµM TNF-alpha and 500 ÂµM IFN-gamma (inflamed) whereas two samples had been left untreated (naive). RNA was prepared using TRIZOL according to standard protocols.

2013-07-08 | E-GEOD-48572 | biostudies-arrayexpress

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