Distinct distal and proximal p53-binding sites in the MCK promoter govern the transcriptional response to p53.
We have investigated the functional importance of nucleotide sequence differences between proximal (P-) and distal (D-) p53-binding elements in the MCK promoter. P- and D-elements normally co-operate to permit synergistic promoter activation by p53. Interestingly, we find that P-elements cannot co-operate with each other. In contrast, co-operation between D-binding sites results in levels of p53-induced transcription far higher than those obtained by co-operation between P- and D-elements. These studies imply that distinct D- and P-p53-binding sites in the MCK promoter may dictate the promoter response to p53.
Jackson
P
P
Oncology Research Centre, Prince of Wales Hospital, Randwick, NSW, Australia. Paul.Jackson@unsw.edu.au
Yardley
G
G
D000818:Animals; D001665:Binding Sites; D002460:Cell Line; D003402:Creatine Kinase / Q000235:genetics*; D000882:Haplorhini; D011401:Promoter Regions, Genetic; D015533:Transcriptional Activation; D014162:Transfection; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
D016159:Tumor Suppressor Protein p53; D003402:Creatine Kinase