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. Author manuscript; available in PMC: 2010 May 1.
Published in final edited form as: J Neurochem. 2009 May;109(Suppl 1):133–138. doi: 10.1111/j.1471-4159.2009.05897.x

Fig. 1.

Fig. 1

Involvement of p53 signaling after ROS generation. After ROS generation from mitochondria, p53 transcriptionally generates pro-apoptotic proteins such as Bax, Noxa, p53AIP1, PUMA, and Bid. These products act directly on mitochondria. Mitochondrial translocation of Bax is promoted by JNK through transcriptional activation of Bim. Full-length PIDD (PIDD-FL) is also transcriptionally upregulated by p53. PIDD-CC, a fragment of PIDD-FL cleaved by autoproteolysis, activates caspase-2 through the formation of the PIDDosome, which precedes Bid truncation and translocation to mitochondria. Moreover, p53 translocates to the mitochondrial membrane and activates the mitochondria-dependent apoptotic pathway in a transcription-independent manner. BH3-only proteins and p53 interact with both pro-apoptotic Bax and anti-apoptotic Bcl-XL on the mitochondrial membrane. This interaction causes Bax oligomerization and activation, which triggers cytochrome c release, leading to neuronal death. tBid, truncated Bid.