| First Author | Ganter B | Year | 1997 |
| Journal | Oncogene | Volume | 15 |
| Issue | 2 | Pages | 193-202 |
| PubMed ID | 9244354 | Mgi Jnum | J:41863 |
| Mgi Id | MGI:894566 | Doi | 10.1038/sj.onc.1201173 |
| Citation | Ganter B, et al. (1997) Myb binding sites within the N-ras promoter repress transcription. Oncogene 15(2):193-202 |
| abstractText | In vitro and in vivo methods were combined to determine the function of the three Myb binding sites (NrasI, NrasII and NrasIII) within the promoter region of the mouse N-ras gene. We found that the c-Myb DNA-binding domain can bind with high affinity to NrasI and NrasII, but with a reduced affinity to NrasIII. In contrast, the full length v-Myb protein from BM2 cells only bound to the middle one of the three sites, NrasII. Both c-Myb and v-Myb functioned as repressors and reduce the basal activity of the N-ras promoter by 60%, as determined by transient transfection experiments using different regions of the N-ras promoter. This repression required a functional Myb DNA-binding domain and could not be overcome by fusion to the potent VP16 activation domain. In electrophoretic mobility shift assays, the v-Myb protein is shown to be present in different conformations depending on its binding to the NrasII or the mim-1A site. The v-Myb conformation is thus suggested to play a critical role in the regulation of v-Myb activity. |
