| First Author | Mai S | Year | 1995 |
| Journal | Nucleic Acids Res | Volume | 23 |
| Issue | 1 | Pages | 1-9 |
| PubMed ID | 7870572 | Mgi Jnum | J:22781 |
| Mgi Id | MGI:70669 | Doi | 10.1093/nar/23.1.1 |
| Citation | Mai S, et al. (1995) The c-myc protein represses the lambda 5 and TdT initiators. Nucleic Acids Res 23(1):1-9 |
| abstractText | The lambda 5 promoter initiates transcription at multiple sites and confers expression in all cell types. Two lambda 5 promoter-derived oligonucleotides (Inr lambda 5:1 and Inr lambda 5:2), each with a transcription start site, could promote transcription in transient transfection assays. In contrast, a third oligonucleotide (+90 lambda 5), without a transcription initiation site, was inactive. The Inr lambda 5:1 and Inr lambda 5:2 oligonucleotides formed a major DNA-protein complex B' in gel retardation analyses; no protein-DNA complexes were observed with the inactive +90 lambda 5 oligonucleotide. The B' complexes of Inr lambda 5:1 and Inr lambda 5:2 each contained c-myc and myn (murine homologue of Max) proteins. The c-myc and myn proteins were also found to bind the TdT initiator (InrTdT). Using mutated oligonucleotides, we found that the c-myc/myn proteins bound to the transcription initiation site of both Inr lambda 5:1 and InrTdT, however, these mutated oligonucleotides were inactive in transfection assays. This suggested that, in this system, transcription depended both on a transcription initiation site and appropriate flanking sequences. The significance of c-myc binding to the respective initiator was analysed by overexpressing c-myc in co-transfection assays. Under these conditions the transcriptional activity of both the lambda 5 and the TdT initiator was repressed. |
