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The p53 tumour suppressor protein is a transcriptional actip53, monomeric variants were not able to induce vator, which can induce cell cycle arrest and apoptosis.apoptosis. We also provided wild-type p53 and p53⌬326 p53 Gene mutations occur in more than 50% of all human with tetracycline-regulated promoters and stably introtumours. Reintroduction of wild-type p53 but also of duced these constructs into Saos2 and SKBR3 cells. Upon oligomerisation-independent p53 variants into tumour cells induction, wild-type p53 expressing cells, but not p53⌬326 by gene transfer methods has been considered. We have expressing cells underwent apoptosis. Consistently, only investigated the biological properties of two carboxy-terwild-type p53 expressing cells accumulated p21/waf1/cip1 minal deletion mutants of p53, p53⌬300 (comprising amino mRNA and protein and showed increased bax, Gadd45 acids 1-300) and p53⌬326 (amino acids 1-326), to evaluand mdm2 mRNA. Neither wild-type p53 nor p53⌬326 ate their potential deployment in gene therapy. Transactivrepressed the transcription of the IGF-1R gene in these ation was measured in transiently transfected HeLa and cell lines. We conclude that the transactivation potential of SKBR3 cells. Both monomeric variants showed reduced monomeric, carboxy-terminally truncated p53 is not sufactivities compared with wild-type p53. Individual proficient to cause induction of the endogenous target genes moters were differently affected. In contrast to wild-type which trigger apoptosis.