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Jane M. Bradbury, Stephen P. Jackson
ATM and ATR Jane M. Bradbury, Stephen P. Jackson Current Biology Volume 13, Issue 12, (June 2003) DOI: /S (03)
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Figure 1 A possible model for the early events in ATM activation. In cells with undamaged DNA (1), ATM exists as dimers/multimers in which the active site is blocked. Double-strand DNA breaks (2) lead to ATM intermolecular phosphorylation (yellow), dissociation of the dimer/multimer and exposure of the kinase domain (3). ATM is then thought to be targeted to DNA lesions via adaptor(s) (4). Focus formation follows the phosphorylation of ATM targets (such as p53, red). The cellular outcome depends on whether successful DNA repair occurs. Current Biology , DOI: ( /S (03) )
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