| First Author | Ishisaki A | Year | 1997 |
| Journal | Eur J Biochem | Volume | 246 |
| Issue | 1 | Pages | 142-6 |
| PubMed ID | 9210476 | Mgi Jnum | J:41005 |
| Mgi Id | MGI:892724 | Doi | 10.1111/j.1432-1033.1997.t01-2-00142.x |
| Citation | Ishisaki A, et al. (1997) Nuclear factor Y controls the basal transcription activity of the mouse platelet-derived-growth-factor beta-receptor gene. Eur J Biochem 246(1):142-6 |
| abstractText | To determine the regulatory mechanism of the expression of the mouse platelet-derived growth factor (PDGF) beta-receptor gene, a 1.9-kb 5' flanking genomic fragment was cloned and analyzed. Site-directed mutagenesis of a CCAAT motif, located 60 bp upstream of the transcriptional-start site, completely abolished the promoter activity [Ballagi, A. E., Ishisaki, A., Nelin, J.-O. & Funa, K. (1995) Biochem. Biophys. Res. Commun. 210, 165-1751. The sequence around the intact CCAAT motif was protected by in vitro DNase-I-footprinting analysis. Electrophoresis-mobility-shift assays with anti-[nuclear factor Y(NF-Y)]Ig revealed binding of the NF-Y complex to the CCAAT box. Furthermore, the double-stranded oligonucleotides corresponding to the sequence around the CCAAT motif were conjugated with DNA-affinity magnetic beads. The binding proteins were affinity purified and identified as the NF-Y transcription factor by western blotting. Our results indicate that NF-Y controls the basal transcription activity of the mouse PDGF beta-receptor gene. |
