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The tumor suppressor p53 plays a central role in cell fate decisions afterDNA damage. Programmed Cell Death 5 (PDCD5) is known to interact with the p53pathway to promote cell apoptosis. Recombinant human PDCD5 can significantlysensitize different cancers to chemotherapies. In the present paper, weconstruct a computational model that includes PDCD5 interactions in the p53signaling network and study the effects of PDCD5 on p53-mediated cell fatedecisions during the DNA damage response. Our results revealed that PDCD5functions as a co-activator of p53 that regulates p53-dependent cell fatedecisions via the mediation of p53 dynamics. The effects of PDCD5 aredose-dependent such that p53 can display either sustained or pulsed dynamics atdifferent PDCD5 levels. Moreover, PDCD5 regulates caspase-3 activation via twomechanisms during the two phases of sustained and pulsed p53 dynamics. Thisstudy provides insights regarding how PDCD5 functions as a regulator of the p53pathway and might be helpful for increasing our understanding of the molecularmechanisms by which PDCD5 can be used to treat cancers.

PDCD5 interacts with p53 and functions as a regulator of p53 dynamics in the DNA damage response