ArticleProceedings of the National Academy of Sciences of the United States of America2000
Abnormal development of Purkinje cells and lymphocytes in Atm mutant mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
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Who cites it
103 citing papers in PubMed, 173 citations in OpenAlex.
- Recent Advances in Therapy for the Neurodegenerative Disorder Ataxia-Telangiectasia.International journal of molecular sciences · 2026Review
- Programmed Clonal Expansion Associated with V(D)J Recombination Drives an ATM-Dependent Vulnerability Underlying Preferential Lymphocyte Depletion and Myeloid Bias Following DNA Damage.bioRxiv : the preprint server for biology · 2026Article
- ATM-kinase deficiency triggers early multi-compartment remodeling of the cerebellar microenvironment.Acta neuropathologica communications · 2026Article
- Nonhomologous end joining-the importance of end tethering and beyond.Genes & development · 2026Review
- Visualization and quantification of rDNA instabilities in mammalian cells and mouse models.Nucleic acids research · 2026Article
- ATM-dependent DNA damage response constrains cell growth and drives clonal hematopoiesis in telomere biology disorders.The Journal of clinical investigation · 2025Article
- A rad50 germline mutation induces tumorigenesis and ataxia-telangiectasia phenotype in a transparent medaka model.PloS one · 2023Article
- Article
- Poor-Quality Vβ Recombination Signal Sequences and the DNA Damage Response ATM Kinase Collaborate to Establish TCRβ Gene Repertoire and Allelic Exclusion.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Loss ofBiomedicines · 2022Article
- Targeting the ATM Kinase to Enhance the Efficacy of Radiotherapy and Outcomes for Cancer Patients.Seminars in radiation oncology · 2022Review
- FATC Domain Deletion Compromises ATM Protein Stability, Blocks Lymphocyte Development, and Promotes Lymphomagenesis.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Elevated inflammatory responses and targeted therapeutic intervention in a preclinical mouse model of ataxia-telangiectasia lung disease.Scientific reports · 2021Article
- The Cancer-Associated ATM R3008H Mutation Reveals the Link between ATM Activation and Its Exchange.Cancer research · 2021Article
- Article
- The Essential DNA Damage Response Complex MRN Is Dispensable for the Survival and Function of Purkinje Neurons.Frontiers in aging neuroscience · 2021Article
- SIRT3, a metabolic target linked to ataxia-telangiectasia mutated (ATM) gene deficiency in diffuse large B-cell lymphoma.Scientific reports · 2020Article
- The recent advances in non-homologous end-joining through the lens of lymphocyte development.DNA repair · 2020Review
- Mitochondria at the crossroads of ATM-mediated stress signaling and regulation of reactive oxygen species.Redox biology · 2020Review
- Article
43 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Motor incoordination, immune deficiencies, and an increased risk of cancer are the characteristic features of the hereditary disease ataxia-telangiectasia (A-T), which is caused by mutations in the ATM gene. Through gene targeting, we have generated a line of Atm mutant mice, Atm(y/y) mice. In contrast to other Atm mutant mice, Atm(y/y) mice show a lower incidence of thymic lymphoma and survive beyond a few months of age. Atm(y/y) mice exhibit deficits in motor learning indicative of cerebellar dysfunction. Even though we found no gross cerebellar degeneration in older Atm(y/y) animals, ectopic and abnormally differentiated Purkinje cells were apparent in mutant mice of all ages. These findings establish that some neuropathological abnormalities seen in A-T patients also are present in Atm mutant mice. In addition, we report a previously unrecognized effect of Atm deficiency on development or maintenance of CD4(+)8(+) thymocytes. We discuss these findings in the context of the hypothesis that abnormal development of Purkinje cells and lymphocytes contributes to the pathogenesis of A-T.
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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.