ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Analysis of the ataxia telangiectasia mutated-mediated DNA damage response in murine cerebellar neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
24 citing papers in PubMed, 41 citations in OpenAlex.
- Formaldehyde initiates memory and motor impairments under weightlessness condition.NPJ microgravity · 2024Review
- Review
- Article
- Article
- Ataxia-telangiectasia mutated plays an important role in cerebellar integrity and functionality.Neural regeneration research · 2023Review
- Accumulation of formaldehyde causes motor deficits in an in vivo model of hindlimb unloading.Communications biology · 2021Article
- Role of the C9ORF72 Gene in the Pathogenesis of Amyotrophic Lateral Sclerosis and Frontotemporal Dementia.Neuroscience bulletin · 2020Review
- Enforced DNA repair enzymes rescue neurons from apoptosis induced by target deprivation and axotomy in mouse models of neurodegeneration.Mechanisms of ageing and development · 2017Article
- Ataxia telangiectasia: a review.Orphanet journal of rare diseases · 2016Review
- Article
- Brain glucose metabolism in adults with ataxia-telangiectasia and their asymptomatic relatives.Brain : a journal of neurology · 2014Article
- EZH2-mediated H3K27 trimethylation mediates neurodegeneration in ataxia-telangiectasia.Nature neuroscience · 2013Article
- Regulation of the DNA damage response on male meiotic sex chromosomes.Nature communications · 2013Article
- Differential regulation of DNA damage response activation between somatic and germline cells in Caenorhabditis elegans.Cell death and differentiation · 2012Article
- Malfunctioning DNA damage response (DDR) leads to the degeneration of nigro-striatal pathway in mouse brain.Journal of molecular neuroscience : MN · 2012Article
- Stable brain ATM message and residual kinase-active ATM protein in ataxia-telangiectasia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Reduced synchronization persistence in neural networks derived from atm-deficient mice.Frontiers in neuroscience · 2011Article
- Cytoplasmic ATM in neurons modulates synaptic function.Current biology : CB · 2009Article
- Differential expression of small heat shock protein 27 (Hsp27) in Ataxia telangiectasia brains.Neurochemical research · 2009Article
- ATM localization and gene expression in the adult mouse eye.Molecular vision · 2009Article
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
The DNA damage response is a network of signaling pathways that affects many aspects of cellular metabolism after the induction of DNA damage. The primary transducer of the cellular response to the double-strand break, a highly cytotoxic DNA lesion, is the nuclear protein kinase ataxia telangiectasia (A-T) mutated (ATM), which phosphorylates numerous effectors that play key roles in the damage response pathways. Loss or inactivation of ATM leads to A-T, an autosomal recessive disorder characterized by neuronal degeneration, particularly the loss of cerebellar granule and Purkinje cells, immunodeficiency, genomic instability, radiosensitivity, and cancer predisposition. The reason for the cerebellar degeneration in A-T is not clear. It has been ascribed by several investigators to cytoplasmic functions of ATM that may not be relevant to the DNA damage response. We set out to examine the subcellular localization of ATM and characterize the ATM-mediated damage response in mouse cerebellar neurons. We found that ATM is essentially nuclear in these cells and that various readouts of the ATM-mediated damage response are similar to those seen in commonly used cell lines. These include the autophosphorylation of ATM, which marks its activation, and phosphorylation of several of its downstream substrates. Importantly, all of these responses are detected in the nuclei of granule and Purkinje cells, suggesting that nuclear ATM functions in these cells similar to other cell types. These results support the notion that the cerebellar degeneration in A-T patients results from defective DNA damage response.
Indexed as
Identifiers
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.