ArticleDNA repair2013
The role of ATM and DNA damage in neurons: upstream and downstream connections.
Article in DNA repair, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 66 citations in OpenAlex.
- N-terminal oligomerization drives HDAC4 nuclear condensation and neurodevelopmental dysfunction inOpen biology · 2025Article
- Argonaute protein assisted drug discovery for miRNA-181c-5p and target gene ATM translation repression: a computational approach.Molecular diversity · 2025Article
- How do neurons live long and healthy? The mechanism of neuronal genome integrity.Frontiers in neuroscience · 2025Review
- Disproportionate Expression of ATM in Cerebellar Cortex During Human Neurodevelopment.Cerebellum (London, England) · 2024Article
- Alzheimer's Disease-Related Epigenetic Changes: Novel Therapeutic Targets.Molecular neurobiology · 2024Review
- Circulating Cell Free DNA and DNA Double-Strand Breakage in Alzheimer's Disease.Journal of Alzheimer's disease reports · 2024Review
- Contributions of circadian clock genes to cell survival in fibroblast models of lithium-responsive bipolar disorder.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2023Article
- DNA Damage Response-Associated Cell Cycle Re-Entry and Neuronal Senescence in Brain Aging and Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Review
- Age- and Lifespan-Dependent Differences in GO Caused DNA Damage inInternational journal of molecular sciences · 2022Article
- Childhood-Onset Movement Disorders Can Mask a Primary Immunodeficiency: 6 Cases of Classical Ataxia-Telangiectasia and Variant Forms.Frontiers in immunology · 2022Article
- DNA Repair Inhibition Leads to Active Export of Repetitive Sequences to the Cytoplasm Triggering an Inflammatory Response.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Increased Abundance of Nuclear HDAC4 Impairs Neuronal Development and Long-Term Memory.Frontiers in molecular neuroscience · 2021Article
- Review
- Polyploidy in the adulteLife · 2020Article
- DNA double-strand breaks: a potential therapeutic target for neurodegenerative diseases.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2019Review
- Histone deacetylase 4 (HDAC4): a new player in anorexia nervosa?Molecular psychiatry · 2019Review
- RAD6B Plays a Critical Role in Neuronal DNA Damage Response to Resist Neurodegeneration.Frontiers in cellular neuroscience · 2019Article
- Inactive Atm abrogates DSB repair in mouse cerebellum more than does Atm loss, without causing a neurological phenotype.DNA repair · 2018Article
- ATM in breast and brain tumors: a comprehensive review.Cancer biology & medicine · 2018Article
- A BRCA1-Dependent DNA Damage Response in the Regenerating Adult Peripheral Nerve Milieu.Molecular neurobiology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
ATM (ataxia-telangiectasia mutated) is a large protein kinase whose best-known function is as a participant in the process of DNA damage repair, specifically lesions that result in double strand breaks. In the cells of the nervous system, however, the symptoms of children with ataxia-telangiectasia and the phenotypes of mice with engineered mutations in their ATM gene argue for a broader range of protein functions. ATM is now appreciated to play a role in vesicle dynamics as well as in the maintenance of the epigenetic code of histone modifications. Finally, the decline of ATM levels with age suggest that late onset neurodegenerative diseases may owe part of their pathogenesis to deficits in ATM signaling. Evidence from the location of HDAC4 in the hippocampal pyramidal cells of the Alzheimer's disease brain supports this hypothesis. These multiple functions of the ATM protein are in keeping with the complex multi-system nature of the symptoms of ataxia-telangiectasia and encourage us to look beyond DNA damage for the full understanding of the disease and its consequences.
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What OpenQuestion holds
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.