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Interferon Regulatory Factor 5 represses mitochondrial matrix protein GHITM to limit macrophage oxidative capacity in early response to obesity [atm]

ABSTRACT: To investigate the involvement of IRF5 in macrophages during obesity-related inflammation, we analyzed adipose-tissue macrophages (ATM) from mice with a myeloid-specific deletion of IRF5 or their wild-type littermates, fed with high fat diet.

ORGANISM(S): Mus musculus

PROVIDER: GSE208648 | GEO | 2022/07/25

REPOSITORIES: GEO

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Interferon Regulatory Factor 5 represses mitochondrial matrix protein GHITM to limit macrophage oxidative capacity in early response to obesity [bmdm]

Project description:To investigate the involvement of IRF5 in macrophages during obesity-related inflammation, we analyzed bone marrow-derived macrophages stimulated for 2 or 24 hours with Lipopolysaccharide (LPS), Palmitate or carrier (bovine serum albumin), from mice with a myeloid-specific deletion of IRF5 or their wild-type littermates.

2022-07-25 | GSE208667 | GEO

Interferon Regulatory Factor 5 represses mitochondrial matrix protein GHITM to limit macrophage oxidative capacity in early response to obesity [atm]

Project description:Interferon Regulatory Factor 5 represses mitochondrial matrix protein GHITM to limit macrophage oxidative capacity in early response to obesity [atm]

| PRJNA860546 | ENA

Modulation of proteostasis counteracts oxidative stress and affects DNA base excision repair capacity in ATM-deficient cells

Project description:Ataxia telangiectasia (A-T) is a syndrome associated with loss of ATM protein function. Neurodegeneration and cancer predisposition, both hallmarks of A-T, are likely to emerge as a consequence of the persistent oxidative stress and DNA damage observed in this disease. Surprisingly however, despite these severe features, a lack of functional ATM is still compatible with early life, suggesting that adaptation mechanisms contributing to cell survival must be in place. Here we address this gap in our knowledge by analysing the process of human fibroblast adaptation to the lack of ATM. We identify profound rearrangement in cellular proteostasis occurring very early on after loss of ATM in order to counter protein damage originating from oxidative stress. Change in proteostasis, however, is not without repercussions. Modulating protein turnover in ATM-depleted cells also has an adverse effect on the DNA base excision repair pathway, the major DNA repair system that deals with oxidative DNA damage. As a consequence, the burden of unrepaired endogenous DNA lesions intensifies, progressively leading to genomic instability. Our study provides a glimpse at the cellular consequences of loss of ATM and highlights a previously overlooked role for proteostasis in maintaining cell survival in the absence of ATM function.

2017-09-04 | PXD006648 | Pride

Panicum virgatum strain:ATM | cultivar:ATM

Project description:Panicum virgatum ATM Resequencing genome sequencing

| PRJNA332580 | ENA

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).

2010-12-20 | E-TABM-1092 | biostudies-arrayexpress

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).

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

ATM keypad - molecular cartography

Project description:LC-MS/MS data from swab sampling of ATM keypad buttons and finger tips of a person who typed a four-digit PIN.

2017-02-22 | MSV000080560 | MassIVE

ATM Loss and Therapeutic Vulnerabilities in Bladder Cancer

Project description:ATM plays a central role in the cellular response to DNA damage and ATM alterations are common in several tumor types including bladder cancer. However, the specific impact of ATM alterations on therapy response in bladder cancer is uncertain. Here, we combine preclinical modeling and clinical analyses to comprehensively define the impact of ATM alterations in bladder cancer. We show that ATM loss is sufficient to increase sensitivity to DNA damaging agents including cisplatin and radiation. Furthermore, ATM loss drives sensitivity to DNA repair targeted agents including PARP and ATR inhibitors. ATM loss alters the immune microenvironment and improves anti-PD1 response in preclinical bladder models but is not associated with improved anti-PD1/PD-L1 response in clinical cohorts. Finally, we show that ATM expression by IHC is strongly correlated with response to chemoradiotherapy. Together these data define a potential role for ATM as a predictive biomarker in bladder cancer.

2023-11-24 | GSE232850 | GEO

Microarray analysis of gene expression in ATM-deficient MEFs

Project description:The expression of interferon-related genes was more enhanced in irradiated ATM-deficient mouse embryonic fibroblasts (MEFs) than in irradiated ATM wild-type MEFs. Nonirradiated-ATM-WT vs Irradiated-ATM-WT vs Nonirradaited-ATM-KO vs IrradiatedATM-KO

2012-06-19 | E-GEOD-23116 | biostudies-arrayexpress

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

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