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PubMed · 11850786

ATM function and telomere stability.

Tej K Pandita
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Abstract

Accumulation of DNA damage has been associated with the onset of senescence and predisposition to cancer. The gene responsible for ataxia telangiectasia (A-T) is ATM (ataxia-telangiectasia mutant), a master controller of cellular pathways and networks, orchestrating the responses to a specific type of DNA damage: the double strand break. Based on the homology of the human ATM gene to the TEL1, MEC1 and rad3 genes of yeast, it has now been demonstrated that mutations in ATM lead to defective telomere maintenance in mammalian cells. While ATM has both nuclear and cytoplasmic functions, this review will focus on its roles in telomere metabolism and how ATM and telomeres serve as controllers of cellular responses to DNA damage.

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Ataxia TelangiectasiaAtaxia Telangiectasia Mutated ProteinsCell CycleCell Cycle ProteinsChromatinDNA-Binding ProteinsHumansModels, BiologicalMutationNeoplasmsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-ablSignal TransductionTelomeraseTelomereTumor Suppressor ProteinsJournal ArticleResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.Review

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Tej K Pandita. 2002-01-21. ATM function and telomere stability.. https://doi.org/10.1038/sj.onc.1205060

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Use of the cytokinesis-block micronucleus assay to measure radiation-induced chromosome damage in lymphoblastoid cell lines.

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Ataxia Telangiectasia↗
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Aberrant sensing of extracellular Ca2+ by cultured ataxia telangiectasia fibroblasts.

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