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Inhibition of ATM in Mouse-derived lung fibroblasts

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

ORGANISM(S): Mus musculus

PROVIDER: GSE182731 | GEO | 2024/12/22

REPOSITORIES: GEO

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RNA-Seq of lung fibroblasts of Atm defecient and wildtype mice.

Project description:We applied RNA-Seq on lung fibroblasts derived from Atm defecient as well as wildtype mice to further understand and reveal a novel pathawy involved in the premture senescence caused by the loss of Atm.

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MiRNAs expression data from Atm++ and Atm-- mouse embryonic fibroblasts after DNA damage at various time point

Project description:Atm++ and Atm-- mouse embryonic fibroblasts were treated with DNA damaging agent neocarzinostatin (NCS), and cells were harvested at indicated time points for the microarray analyses of whole-genome miRNAs. To examine how miRNAs are regulated in the DNA damage response, we assessed the genome-wide mature miRNA expression in Atm++ and Atm-- littermate mouse embryonic fibroblasts (MEFs).

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MiRNAs expression data from Atm+/+ and Atm-/- mouse embryonic fibroblasts after DNA damage at various time point

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2010-12-09 | E-GEOD-25916 | biostudies-arrayexpress

Long noncoding RNAs expression data from Atm+/+ and Atm-/- mouse embryonic fibroblasts after DNA damage at various time point

Project description:Atm+/+ and Atm-/- mouse embryonic fibroblasts were treated with or without DNA damaging agent neocarzinostatin (NCS), and cells were harvested after 4 hours and 8 hours for the microarray analyses of whole-genome long noncoding RNAs. To examine how long noncoding RNAs are regulated in the DNA damage response, we assessed the genome-wide long noncoding RNA expression in Atm+/+ and Atm-/- littermate mouse embryonic fibroblasts (MEFs) treated with or without DNA damage

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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.

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Inhibition of ATM in Mouse-derived lung fibroblasts

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

| PRJNA757628 | ENA

MiRNAs expression data from Atm+/+ and Atm-/- mouse embryonic fibroblasts after DNA damage at various time point

2010-12-09 | GSE25916 | GEO

Long noncoding RNAs expression data from Atm+/+ and Atm-/- mouse embryonic fibroblasts after DNA damage at various time point

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OncoScan analysis to investigate CNV in breast tumors developed by ATM mutation carriers

Project description:The ataxia telangiectasia-mutated (ATM) gene is a moderate-risk breast cancer susceptibility gene; germline loss-of-function variants are found in up to 3% of hereditary breast and ovarian cancer (HBOC) families who undergo genetic testing. So far, no clear molecular features of breast tumors occuring in ATM deleterious variant carriers have been described, but identification of an ATM-associated tumors signature may help patients' management. To characterize hallmarks of ATM-associated tumors, absolute copy number variation and loss of heterozygosity profiles were obtained from the OncoScan SNP array.

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Inhibition of the ATM kinase rescues planarian regeneration after lethal radiation

Project description:As stem cells divide, they acquire mutations that can be passed on to daughter cells. To mitigate potentially deleterious outcomes, cells activate the DNA damage response (DDR) network, which governs several potential cellular outcomes following DNA damage, including repairing DNA or undergoing apoptosis. At the helm of the DDR are three PI3-like kinases including Ataxia Telangiectasia Mutated (ATM). We report here that knockdown of ATM in planarian flatworms enables stem cells to withstand lethal doses of radiation which would otherwise induce cell death. In this context, stem cells circumvent apoptosis, replicate their DNA, and recover function using homologous recombination-mediated DNA repair. Despite radiation exposure, atm knockdown animals survive long-term and regenerate new tissues. These effects occur independently of ATM’s canonical downstream effector p53. Together, our results demonstrate that in planarians, ATM regulates radiation-induced apoptosis. This acute, ATM-dependent apoptosis is a key determinant of long-term animal survival. Our results suggest that inhibition of ATM in these organisms could therefore potentially favor cell survival after radiation without obvious effects on stem cell behavior.

2022-12-25 | GSE190454 | GEO

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