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. Author manuscript; available in PMC: 2013 Dec 11.
Published in final edited form as: FEBS Lett. 2011 May 19;585(18):10.1016/j.febslet.2011.04.078. doi: 10.1016/j.febslet.2011.04.078

Figure 2.

Figure 2

Deactivation of the Fanconi anemia pathway by deubiquitylation

The signaling that takes place in the activation of DNA repair must be attenuated when DNA repair has concluded. The ID complex is deubiquitylated by USP1 whose activity is enhanced by interaction with UAF1. USP1 has a parallel role in the deubiquitylation of PCNA. USP1/UAF1 substrate affinity is regulated by auxiliary factors such as ELG1, which is required for the deubiquitylation of PCNA specifically. The DUBs are themselves subject to regulation on both a transcriptional and post-transcriptional level. Importantly, USP1 is polyubiquitylated as DNA replication concludes. Polyubiquitylated USP1 is targeted for proteasomal degradation.

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