ArticlePloS one2014
The interaction of the atm genotype with inflammation and oxidative stress.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- A dual role for cGAS in shaping cellular and organismal responses to genomic instability.Genes & development · 2026Article
- Computational modeling of ATM signaling: a predictive framework for drug repurposing in ataxia-telangiectasia.NPJ systems biology and applications · 2025Article
- Germline-Somatic Interactions in BRCA-Associated Cancers: Unique Molecular Profiles and Clinical Outcomes Linking ATM to TP53 Synthetic Essentiality.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- Review
- DNA damage, inflammation and aging: Insights from mice.Frontiers in aging · 2022Review
- Altered Cerebrospinal Fluid (CSF) in Children with Ataxia Telangiectasia.Cerebellum (London, England) · 2021Article
- Review
- Accumulation of Cytoplasmic DNA Due to ATM Deficiency Activates the Microglial Viral Response System with Neurotoxic Consequences.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Testing the Neuroprotective Properties of PCSO-524Marine drugs · 2019Article
- Progressive Liver Disease in Patients With Ataxia Telangiectasia.Frontiers in pediatrics · 2019Article
- Inactive Atm abrogates DSB repair in mouse cerebellum more than does Atm loss, without causing a neurological phenotype.DNA repair · 2018Article
- Ibuprofen prevents progression of ataxia telangiectasia symptoms in ATM-deficient mice.Journal of neuroinflammation · 2018Article
- Inflammation, a significant player of Ataxia-Telangiectasia pathogenesis?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Review
- The impact of glutamine supplementation on the symptoms of ataxia-telangiectasia: a preclinical assessment.Molecular neurodegeneration · 2016Article
- Article
- Non-Neuronal Cells Are Required to Mediate the Effects of Neuroinflammation: Results from a Neuron-Enriched Culture System.PloS one · 2016Article
- A novel mouse model for ataxia-telangiectasia with a N-terminal mutation displays a behavioral defect and a low incidence of lymphoma but no increased oxidative burden.Human molecular genetics · 2015Article
- Physiological and pathophysiological functions of cell cycle proteins in post-mitotic neurons: implications for Alzheimer's disease.Acta neuropathologica · 2015Review
- Correction: The Interaction of the Atm Genotype with Inflammation and Oxidative Stress.PloS one · 2015Article
- Ataxia-telangiectasia clinical trial landscape and the obstacles to overcome.Expert opinion on investigational drugsReview
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
In ataxia-telangiectasia (A-T) the death of neurons is associated with the loss of neuronal cell cycle control. In most Atm(-/-) mouse models, however, these cell cycle anomalies are present but the phenotype of neuronal cell loss found in humans is not. Mouse Atm(-/-) neurons re-enter a cell cycle and replicate their DNA, but they do not die--even months after initiating the cycle. In the current study, we explore whether systemic inflammation or hypoxia-induced oxidative stress can serve as second stressors that can promote cell death in ATM-deficient neurons. We find that after either immune or hypoxic challenge, the levels of cell cycle proteins--PCNA, cyclin A and cyclin B--are significantly elevated in cerebellar Purkinje cells. Both the number of cells that express cell cycle proteins as well as the intensity of the expression levels in each cell is increased in the stressed animals. The cell cycle-positive neurons also increasingly express cell death markers such as activated caspase-3, γ-H2AX and TUNEL staining. Interestingly, nuclear HDAC4 localization is also enhanced in Atm(-/-) Purkinje neurons after the immune challenge suggesting that both genetic and epigenetic changes in Atm(-/-) mice respond to environmental challenges. Our findings support the hypothesis that multiple insults are needed to drive even genetically vulnerable neurons to die a cell cycle-related cell death and point to either inflammation or oxidative stressors as potential contributors to the A-T disease process.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.