The activated form of p53 is not a transactivator of the intracisternal A particle long terminal repeat promoter.
Published observations have suggested that the activated form of p53 protein could transactivate the Intracisternal A particle long terminal repeat promoter (IAP-LTR). In this paper we demonstrate that the increased expression from this promoter was due to effects of the co-transferred plasmids and not p53 per se. In transient expression experiments, co-transfer of either a p53 or a p53 frame-shift mutant plasmid with an IAP-LTR driven chloramphenicol acetyl transferase (CAT) plasmid gave a similar increase in CAT activity. Further, this increase in CAT gene activity could also be achieved by co-transfer of a plasmid containing a viral promoter alone.
Mowat
M
M
Manitoba Institute of Cell Biology, Winnipeg, Canada.
Sauder
M
M
Pereira
D
D
D015500:Chloramphenicol O-Acetyltransferase / Q000032:analysis / Q000235:genetics; D007426:Genes, Intracisternal A-Particle; D006801:Humans; D015513:Oncogene Proteins / Q000502:physiology*; D010750:Phosphoproteins / Q000502:physiology*; D010957:Plasmids; D011401:Promoter Regions, Genetic; D011519:Proto-Oncogenes; D012091:Repetitive Sequences, Nucleic Acid; D015534:Trans-Activators / Q000502:physiology*; D016159:Tumor Suppressor Protein p53
D015513:Oncogene Proteins; D010750:Phosphoproteins; D015534:Trans-Activators; D016159:Tumor Suppressor Protein p53; D015500:Chloramphenicol O-Acetyltransferase