DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation
Abstract
The ATM protein kinase, mutations of which are associated with the human disease ataxia-telangiectasia, mediates responses to ionizing radiation in mammalian cells. Here we show that ATM is held inactive in unirradiated cells as a dimer or higher-order multimer, with the kinase domain bound to a region surrounding serine 1981 that is contained within the previously described 'FAT' domain. Cellular irradiation induces rapid intermolecular...
Paper Details
Title
DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation
Published Date
Jan 1, 2003
Journal
Volume
421
Issue
6922
Pages
499 - 506
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