DNA damage- and stress-induced apoptosis occurs independently of PIDD

Ira R. Kim, Kiichi Murakami, Nien Jung Chen, Samuel D. Saibil, Elzbieta Matysiak-Zablocki, Alisha R. Elford, Madeleine Bonnard, Samuel Benchimol, Andrea Jurisicova, Wen Chen Yeh, Pamela S. Ohashi

Research output: Contribution to journalArticlepeer-review

43 Scopus citations


The p53-induced protein with a death domain, PIDD, was identified as a p53 target gene whose main role is to execute apoptosis in a p53-dependent manner. To investigate the physiological role of PIDD in apoptosis, we generated PIDD-deficient mice. Here, we report that, although PIDD expression is inducible upon DNA damage, PIDD-deficient mice undergo apoptosis normally not only in response to DNA damage, but also in response to various p53-independent stress signals and to death receptor (DR) engagement. This indicates that PIDD is not required for DNA damage-, stress-, and DR-induced apoptosis. Also, in the absence of PIDD, both caspase-2 processing and activation occur in response to DNA damage. Our findings demonstrate that PIDD does not play an essential role for all p53-mediated or p53-independent apoptotic pathways.

Original languageEnglish
Pages (from-to)1039-1049
Number of pages11
Issue number9
StatePublished - Sep 2009


  • Apoptosis
  • Caspase-2
  • Gene-targeting
  • P53
  • PIDD


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