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PubMed · 16774833

The ATM-mediated DNA-damage response: taking shape.

Yosef Shiloh
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Abstract

Cellular responses to DNA damage are crucial for maintaining homeostasis and preventing the development of cancer. Our understanding of the DNA-damage response has evolved: whereas previously the focus was on DNA repair, we now appreciate that the response to DNA lesions involves a complex, highly branched signaling network. Defects in this response lead to severely debilitating, cancer-predisposing "genomic instability syndromes". Double strand breaks (DSBs) in DNA are potent triggers of the DNA-damage response, which is why they are used to study this pathway. The chief transducer of the DSB signal is the nuclear protein kinase ataxia-telangiectasia mutated (ATM). Genetic, biochemical and structural studies have recently provided insights into the ATM-mediated DSB response, reshaping our view of this signaling pathway while raising new questions.

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Acid Anhydride HydrolasesAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCyclic AMP Response Element-Binding ProteinDNA DamageDNA RepairDNA Repair EnzymesDNA-Binding ProteinsHumansIntracellular Signaling Peptides and ProteinsMRE11 Homologue ProteinModels, BiologicalPhosphoproteinsProtein Serine-Threonine KinasesTumor Suppressor ProteinsTumor Suppressor p53-Binding Protein 1Xenopus ProteinsJournal ArticleResearch Support, N.I.H., ExtramuralResearch Support, Non-U.S. Gov't

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BibTeXRIS

Yosef Shiloh. 2006-06-13. The ATM-mediated DNA-damage response: taking shape.. https://doi.org/10.1016/j.tibs.2006.05.004

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