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. Author manuscript; available in PMC: 2015 Sep 8.
Published in final edited form as: Oncogene. 2012 Jan 23;31(45):4733–4739. doi: 10.1038/onc.2011.639

Figure 2.

Figure 2

Cellular responses reported to engage PIDD. PIDD is induced in response to DNA damage in a p53-dependent manner, and depending on the type and severity of the damage is recruited to different complexes. A low amount of DNA damage leads to autoproteolytical cleavage of full length PIDD to the PIDD-C form. This fragment associates with NEMO and receptor interacting protein (RIP-1), thereby facilitating postranslational modifications on NEMO leading to activation of NFκB. After more severe genotoxic stress, PIDD-C is further autoproteolytically cleaved to the PIDD-CC fragment, which can bind to RAIDD and caspase-2, which is subsequently processed and activated. In response to UV-IR, PIDD-C can displace p21 from proliferating cell nuclear antigen (PCNA), thereby facilitating recruitment of the translesion synthesis repair machinery.