p63 and p73 express two main classes of isoforms: isoforms which contain the 
transactivation domain (TAp73 and TAp63) executing transcriptional activity and 
dominant-negative isoforms which are truncated at the NH2-terminus acting as 
operant inhibitors of TAp73, TAp63 and wild-type p53, and thus possessing 
oncogenic potential. Like wt p53, TAp63 and TAp73 isoforms transactivate target 
genes that activate apoptosis signaling pathways. In an attempt to understand 
how the CD95 gene is regulated by the p53 family, we investigated the 
contributions of a p53-responsive element (RE) within the first intron of the 
CD95 gene as well as three elements within the promoter. The intronic element 
conferred transcriptional activation by p53, TAp63 and TAp73 and cooperated with 
the p53-REs in the promoter of the CD95 gene. Cooperation between the p53-REs in 
the promoter and the intronic p53-binding site resulted in maximal 
transcriptional activation of the CD95 gene by the p53 family.