Figure 1. Speculative model depicting the TIRR/53BP1 dissociation in response to γ-radiation. In undamaged cells, 2 53BP1 molecules interact with a dimer of TIRR via their Tudor domain and possibly their N-terminal extremity. Following g-irradiation (IR), ATM-dependent phosphorylation of 53BP1 N-terminal extremity weakens the interaction of TIRR with 53BP1 and further promotes the recruitment of RIF1 on 53BP1 leading to the release of TIRR from 53BP1.
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