ReviewJournal of clinical immunology1996
Ataxia-telangiectasia and the ATM gene: linking neurodegeneration, immunodeficiency, and cancer to cell cycle checkpoints.
Review in Journal of clinical immunology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 80 citations in OpenAlex.
- Hypoxia facilitates triple-negative breast cancer stem cells enrichment and stemness maintenance through oxidized ataxia telangiectasia mutated-induced one-carbon metabolism.World journal of stem cells · 2026Article
- How do neurons live long and healthy? The mechanism of neuronal genome integrity.Frontiers in neuroscience · 2025Review
- Shared brain transcriptomic signature in TDP-43 type A FTLD patients with or without GRN mutations.Brain : a journal of neurology · 2022Article
- Progressive choreodystonia in X-linked hyper-IgM immunodeficiency: a rare but recurrent presentation.Annals of clinical and translational neurology · 2022Article
- R-loop Mediated DNA Damage and Impaired DNA Repair in Spinal Muscular Atrophy.Frontiers in cellular neuroscience · 2022Review
- Type I interferon (IFN)-inducible Absent in Melanoma 2 proteins in neuroinflammation: implications for Alzheimer's disease.Journal of neuroinflammation · 2019Review
- From yeast to humans: Understanding the biology of DNA Damage Response (DDR) kinases.Genetics and molecular biology · 2019Article
- The Major Tegument Protein of Bovine Herpesvirus 1, VP8, Interacts with DNA Damage Response Proteins and Induces Apoptosis.Journal of virology · 2018Article
- RAD52 is required for RNA-templated recombination repair in post-mitotic neurons.The Journal of biological chemistry · 2018Article
- Topoisomerase I in Human Disease Pathogenesis and Treatments.Genomics, proteomics & bioinformatics · 2016Review
- Dysregulation of the DNA Damage Response and KMT2A Rearrangement in Fetal Liver Hematopoietic Cells.PloS one · 2015Article
- A novel tumor suppressor function of Kindlin-3 in solid cancer.Oncotarget · 2014Article
- Ataxia-telangiectasia: future prospects.The application of clinical genetics · 2014Review
- ISG15 deregulates autophagy in genotoxin-treated ataxia telangiectasia cells.The Journal of biological chemistry · 2013Article
- Article
- The role of the DNA damage response kinase ataxia telangiectasia mutated in neuroprotection.The Yale journal of biology and medicine · 2012Review
- Malignant melanoma, breast cancer and other cancers in patients with Parkinson's disease.International journal of cancer · 2012Article
- Cancer and neurodegeneration: between the devil and the deep blue sea.PLoS genetics · 2010Review
- Somatic mutations of the Parkinson's disease-associated gene PARK2 in glioblastoma and other human malignancies.Nature genetics · 2010Article
- Oxidative stress is linked to ERK1/2-p16 signaling-mediated growth defect in ATM-deficient astrocytes.The Journal of biological chemistry · 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Defects in regulation of the cellular life cycle may lead to premature cellular death or malignant transformation. Most of the proteins known to be involved in these processes are mediators of mitogenic signals or components of the cell cycle machinery. It has recently become evident, however, that systems responsible for ensuring genome stability and integrity are no less important in maintaining the normal life cycle of the cell. These systems include DNA repair enzymes and a recently emerging group of proteins that alert growth regulating mechanisms to the presence of DNA damage. These signals slow down the cell cycle while DNA repair ensues. Ataxia telangiectasia (A-T) is a genetic disorder whose clinical and cellular phenotype points to a defect in such a signaling system. A-T is characterized by neurodegeneration, immunodeficiency, radiosensitivity, cancer predisposition, and defective cell cycle checkpoints. The responsible gene, ATM, was recently cloned and sequenced. ATM encodes a large protein with a region highly similar to the catalytic domain of PI 3-kinases. The ATM protein is similar to a group of proteins in various organisms which are directly involved in the cell cycle response to DNA damage. It is expected to be part of a protein complex that responds to a specific type of DNA strand break by conveying a regulatory signal to other proteins. Interestingly, the immune and nervous systems, which differ markedly in their proliferation rates, are particularly sensitive to the absence of ATM function. The identification of the ATM gene highlights the growing importance of signal transduction initiated in the nucleus rather than in the external environment, for normal cellular growth.
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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.