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ATM interactome and analysis of its substrates

ABSTRACT: Study of ATM interactome and its substrates following pull-down with anti -pSQ/TQ antibody

INSTRUMENT(S): Orbitrap Exploris 480, Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Fibroblast

DISEASE(S): Disease Free

SUBMITTER: angela cattaneo

LAB HEAD: angela bachi

PROVIDER: PXD032194 | Pride | 2024-01-24

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	GB_MF_210209_DMSO.raw	Raw
	GB_MF_210209_DMSO_r.raw	Raw
	GB_MF_210209_Jaspa.raw	Raw
	GB_MF_210209_Jaspa_ATMi.raw	Raw
	GB_MF_210209_Jaspa_ATMi_r.raw	Raw

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1 - 5 of 39

Publications

Cell stretching activates an ATM mechano-transduction pathway that remodels cytoskeleton and chromatin.

Bastianello Giulia G Porcella Giancarlo G Beznoussenko Galina V GV Kidiyoor Gururaj G Ascione Flora F Li Qingsen Q Cattaneo Angela A Matafora Vittoria V Disanza Andrea A Quarto Micaela M Mironov Alexander A AA Oldani Amanda A Barozzi Sara S Bachi Angela A Costanzo Vincenzo V Scita Giorgio G Foiani Marco M

Cell reports 20231211 12

Ataxia telangiectasia mutated (ATM) and ataxia telangiectasia and Rad3-related (ATR) DNA damage response (DDR) kinases contain elastic domains. ATM also responds to reactive oxygen species (ROS) and ATR to nuclear mechanical stress. Mre11 mediates ATM activation following DNA damage; ATM mutations cause ataxia telangiectasia (A-T). Here, using in vivo imaging, electron microscopy, proteomic, and mechano-biology approaches, we study how ATM responds to mechanical stress. We report that cytoskelet ...[more]

PMID: 38088930

Similar Datasets

12-month-old ATM-null mouse cerebellar transcriptome

Project description:In cerebellar atrophy of 12-month-old ATM-null mice, transcriptome upregulations concern most neurotransmission and neuropeptide pathways, while downregulations affect prominently Itpr1, Usp2 and non-coding RNA In cerebellar atrophy of 12-month-old ATM-null mice, transcriptome upregulations concern most neurotransmission and neuropeptide pathways, while downregulations affect prominently Itpr1, Usp2 and non-coding RNA The autosomal recessive disorder Ataxia-Telangiectasia is caused by dysfunction of stress response protein ATM. In the nucleus of proliferating cells, ATM senses DNA double-strand breaks and coordinates their repair. This role explains T-cell dysfunction and tumor risk. However, it remains unclear whether this function is relevant for postmitotic neurons and underlies the cerebellar atrophy, since ATM is cytoplasmic in postmitotic neurons. Here, we used ATM-null mice that survived early immune deficits by bone-marrow transplantation, and reached initial neurodegeneration stages at 12 months of age. Global cerebellar transcriptomics demonstrated ATM depletion to trigger upregulations in most neurotransmission and neuropeptide systems. Downregulated transcripts were found for the ATM interactome component Usp2, many non-coding RNAs, ataxia genes Itpr1, Grid2, immediate early genes and immunity factors. Allelic splice changes affected prominently neuropeptide machinery, e.g. Oprm1. Validation experiments with stressors were performed in human neuroblastoma cells, where ATM localized only to cytoplasm, similar to brain. Effect confirmation in SH-SY5Y cells occurred better after ATM depletion and osmotic stress better than nutrient / oxidative stress, rather than ATM kinase inhibition or DNA stressor bleomycin. Overall, we provide pioneer observations from a faithful A-T mouse model, which suggest general changes in synaptic and dense-core vesicle stress adaptation.

2023-10-24 | GSE241955 | GEO

ATM INDUCES MACROD2 NUCLEAR EXPORT UPON DNA DAMAGE

Project description:ADP-ribosylation is a dynamic post-translation modification that regulates the early phase of various DNA repair pathways by recruiting repair factors to chromatin. ADP-ribosylation levels are defined by the activities of transferases and hydrolases. Little is known about regulation of these enzymes except for that of the transferase ARTD1/PARP1. Among the hydrolases, MacroD2 contains a unique C-terminal region, which may regulate the enzymatic activity carried out by the N-terminal macrodomain. Our study shows that MacroD2 is exported from the nucleus upon DNA damage, and that this nuclear export is induced by ATM activity. In the MacroD2 C-terminal unstructured region we find two SQ/TQ motifs that are necessary for this regulation, arguing for a direct interaction with ATM. This study also shows that MacroD2 nuclear export restricts MacroD2 recruitment to the DNA damage site on the temporal scale, suggesting that the regulation of location determines a regulation of enzymatic activity.

2016-10-12 | PXD003712 | Pride

RNA interactome capture in E. coli to identify RNA-binding proteins

Project description:RNA-binding proteins (RPBs) are deeply involved in fundamental cellular processes in bacteria and are vital for their survival. Despite this, few studies have so far been dedicated to globally identifying bacterial RBPs. We have adapted the RNA interactome capture (RIC) technique, originally developed for eukaryotic systems, to globally identify RBPs in bacteria. RIC takes advantage of the base pairing potential of poly(A) tails to pull-down mRNA-protein complexes. By overexpressing poly(A) polymerase I, we drastically increase the fraction of polyadenylated RNA in Escherichia coli, allowing us to pull-down RNA-protein complexes using immobilized oligo-d(T) as bait. With this approach, we identified 169 putative RBPs, roughly half of which are already annotated as RNA-binding

2022-11-13 | GSE217569 | GEO

Panicum virgatum strain:ATM | cultivar:ATM

Project description:Panicum virgatum ATM Resequencing genome sequencing

| PRJNA332580 | ENA

ATM regulates a DNA damage response post-transcriptional RNA operon in lymphocytes

Project description:Maintenance of genomic stability depends on the DNA damage response (DDR), a biological barrier in early stages of cancer development. Failure of this response results in genomic instability and high predisposition toward lymphoma, as seen in patients with ataxia-telangiectasia mutated (ATM) dysfunction. ATM activates multiple cell cycle checkpoints and DNA repair following DNA damage, but its influence on posttranscriptional gene expression has not been examined on a global level. We show that ionizing radiation (IR) modulates the dynamic association of the RNA-binding protein HuR with target mRNAs in an ATM-dependent manner, potentially coordinating the genotoxic response as an RNA operon. Pharmacologic ATM inhibition and use of ATM-null cells revealed a critical role for ATM in this process. Numerous mRNAs encoding cancer-related proteins were differentially associated with HuR depending on the functional state of ATM, in turn affecting expression of encoded proteins. The findings presented here reveal a previously unidentified role of ATM in controlling gene expression post-transcriptionally. Dysregulation of this DDR RNA operon is likely relevant to lymphoma development in ataxia-telangiectasia individuals. These novel RNA regulatory modules and genetic networks provide critical insight into the function of ATM in oncogenesis. B-lymphocyte cell lines GM02184 (wild type, ATM +/+) and GM03332 (AT, ATM -/-) were either untreated or exposed to 1 Gy of IR. 6 h later cells were harvested and used for immunoprecipitation (IP) in the presence of HuR antibody (Santa Cruz Biotech.). RNA from IP material was extracted and used for microarray analysis.

2011-01-05 | E-GEOD-25848 | 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).

2010-12-20 | 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

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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