Bird R Curtis, Deinnocentes Patricia
Department of Pathobiology, College of Veterinary Medicine, Auburn University, Auburn, AL 36849-5519, USA.
Anticancer Res. 2004 May-Jun;24(3a):1469-80.
Transcription of CDK1 is induced at the G0/G1-phase of the cell cycle and after okadaic acid treatment and we identified the Site I okadaic acid response element (OARE -944 to -763nt) enhancer in the human CDK1 promoter.
The OARE region of the CDK1 promoter was characterized for enhancer/repressor activities.
Transient transfection of upper and lower Site I subregions suggested enhanced transcription activity was divided between both while mobility shift assays demonstrated sequence-specific protein binding to Site IA. Site IA also formed shift complexes following serum starvation/refeeding and putative transcription factor binding sites clustered in Site IA. Oligonucleotides encoding a consensus CDP transcription factor binding site effectively competed against authentic Site IA in mobility shift assays. Mutation of the CDP-like binding sequence substantially reduced competition. DNaseI footprinting revealed binding at this site.
The CDP-like recognition sequence appears to comprise the OARE binding authentic CDP and/or related factors. We termed this site the CDK1 transcription activation sequence-1 (CTAS-1) enhancer of the human CDK1 promoter.