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. 2005 Dec 2;7(2):154–160. doi: 10.1038/sj.embor.7400629

Figure 2.

Figure 2

Ataxia-telangiectasia-mutated activates checkpoint arrest to facilitate the repair of double-stranded breaks regulated by Artemis. A model is provided showing the different pathways for the rejoining of different forms of double-stranded breaks (DSBs). A direct break creating 3′OH and 5′P ends in response to radiation damage is readily repaired by ligation (on the left). This is also the case for signal ends generated during V(D)J recombination (on the right). More complex breaks or ends not amenable to direct ligation require ataxia-telangiectasia mutated (ATM)-dependent processing and the involvement of a series of other proteins including Artemis. NHEJ, non-homologous end joining. Figure provided by P. Jeggo, modified from Löbrich & Jeggo (2005).