The p53 protein is an important tumor suppressor that regulates many cellular processes including maintenance of the cell cycle and apoptosis. The p53 protein maintains stability of the genome through the induction of several intracellular and extracellular factors in response to DNA damage, which in turn, stabilizes the protein, allowing it to undergo its proper mechanisms of action. We recently reported that the p53 tumor suppressor gene has a bidirectional gene partner, Wrap53β. This discovery prompted the development of a bidirectional expression vector system (pLucRLuc) that is capable of measuring the output of transcripts mediated by bidirectional promoters. We have begun to study the nature of the p53/Wrap53β promoters. Here, we have continued these studies by incorporating mutations within the regulatory regions of the p53/Wrap53β bidirectional gene pair to study the effect(s) these have on the two promoters. Deletions and point mutations were created within the two promoters and their activity was examined in the pLucRLuc system. Our results demonstrated that each of the deleted sequences within the murine p53/Wrap53β promoters reduced the activity of each of the promoters. Co-transfections with the pLucRLuc:p53/Wrap53β bidirectional expression vector and known p53 transcriptional regulators were also performed. Here, we demonstrate that p53's bidirectional gene partner, Wrap53β, can also be regulated by many of the same transcription factors.
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