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. 2005 Jan 27;24(4):836–848. doi: 10.1038/sj.emboj.7600444

Figure 8.

Figure 8

Itch controls p73 levels in resting conditions and in response to DNA damage. (A) Schematic representation of the functional interaction between p73 and Itch. Under nonstressed conditions, basal levels of both TAp73 and ΔNp73 are kept low; in this situation, Itch binds to p73 and promotes its ubiquitination and proteasome-dependent degradation. (B) In response to DNA damage, Itch is rapidly degraded, reducing p73 turn over. TAp73 levels increase while ΔNp73 remain low due to the activation of a DNA damage-dependent ΔN-specific degradation pathway. The final outcome is the induction of cell cycle arrest and apoptosis by p73.