ArticleCurrent biology : CB2009
Cytoplasmic ATM in neurons modulates synaptic function.
Article in Current biology : CB, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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.
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Who cites it
68 citing papers in PubMed, 143 citations in OpenAlex.
- ATM-kinase deficiency triggers early multi-compartment remodeling of the cerebellar microenvironment.Acta neuropathologica communications · 2026Article
- Proteomic sensors for quantitative multiplexed and spatial monitoring of kinase signaling.Nature communications · 2025Article
- Diffusion of activated ATM explains γH2AX and MDC1 spread beyond the DNA damage site.iScience · 2024Article
- The DNA repair protein DNA-PKcs modulates synaptic plasticity via PSD-95 phosphorylation and stability.EMBO reports · 2024Article
- The DNA damage sensor ATM kinase interacts with the p53 mRNA and guides the DNA damage response pathway.Molecular cancer · 2024Article
- Article
- Review
- Ataxia-telangiectasia mutated plays an important role in cerebellar integrity and functionality.Neural regeneration research · 2023Review
- ATM rules neurodevelopment and glutamatergic transmission in the hippocampus but not in the cortex.Cell death & disease · 2022Article
- Tracing brain genotoxic stress in Parkinson's disease with a novel single-cell genetic sensor.Science advances · 2022Article
- Exocytosis Proteins: Typical and Atypical Mechanisms of Action in Skeletal Muscle.Frontiers in endocrinology · 2022Review
- ATM Modulates Nuclear Mechanics by Regulating Lamin A Levels.Frontiers in cell and developmental biology · 2022Article
- Cellular functions of the protein kinase ATM and their relevance to human disease.Nature reviews. Molecular cell biology · 2021Review
- A novel, ataxic mouse model of ataxia telangiectasia caused by a clinically relevant nonsense mutation.eLife · 2021Article
- ATM loss disrupts the autophagy-lysosomal pathway.Autophagy · 2021Article
- ATR regulates neuronal activity by modulating presynaptic firing.Nature communications · 2021Article
- The DNA repair protein ATM as a target in autism spectrum disorder.JCI insight · 2021Article
- Alternative Functions of Cell Cycle-Related and DNA Repair Proteins in Post-mitotic Neurons.Frontiers in cell and developmental biology · 2021Article
- DNA damage in human glomerular endothelial cells induces nodular glomerulosclerosis via an ATR and ANXA2 pathway.Scientific reports · 2020Article
- The role of AMPK in metabolism and its influence on DNA damage repair.Molecular biology reports · 2020Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
ATM is a PI 3-kinase involved in DNA double-strand break repair. ATM deficiency leads to ataxia-telangiectasia (A-T), a syndrome of cancer susceptibility, hypersensitivity to ionizing radiation, immune deficiency, and sterility [1, 2]-phenotypes that can straightforwardly be attributed to a defective response to DNA damage. Yet patients with A-T also suffer from ataxia, speech defects, and abnormal body movements [3-5]-neurological phenotypes whose origins remain largely unexplained. Compounding the discordance, Atm mutations in mouse interfere with DNA repair but have only mild neurological symptoms [6-9], suggesting that the link between DNA damage and the death of neurons can be broken [10-12]. We find that in neurons, ATM protein has a substantial cytoplasmic distribution. We show that in Atm(tm1Awb) mice, hippocampal long-term potentiation is significantly reduced, as is the rate of spontaneous vesicular dye release, suggesting a functional importance of cytoplasmic ATM. In the cytoplasm, ATM forms a complex with two synaptic vesicle proteins, VAMP2 and synapsin-I, both of which must be phosphorylated to bind ATM. Also, cytoplasmic ATM physically associates with the homologous PI 3-kinase, ATR. The neurological symptoms of ataxia-telangiectasia may thus result from defective nonnuclear functions of ATM not associated with DNA repair.
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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.