ArticleNucleic acids research1995
The c-myc protein represses the lambda 5 and TdT initiators.
Article in Nucleic acids research, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 44 citations in OpenAlex.
- Article
- Article
- Repression of transcription of the p27(Kip1) cyclin-dependent kinase inhibitor gene by c-Myc.Oncogene · 2001Article
- Review article: role of the surrogate light chain and the pre-B-cell receptor in mouse B-cell development.Immunology · 2000Review
- Coexamination of site-specific transcription factor binding and promoter activity in living cells.Molecular and cellular biology · 1999Article
- Myc-mediated transformation: the repression connection.Oncogene · 1999Review
- Differential effects of the widely expressed dMax splice variant of Max on E-box vs initiator element-mediated regulation by c-Myc.Oncogene · 1999Article
- Analysis of mice with single and multiple copies of transgenes reveals a novel arrangement for the lambda5-VpreB1 locus control region.Molecular and cellular biology · 1999Article
- c-Myc target genes involved in cell growth, apoptosis, and metabolism.Molecular and cellular biology · 1999Review
- The Myc negative autoregulation mechanism requires Myc-Max association and involves the c-myc P2 minimal promoter.Molecular and cellular biology · 1997Article
- A link between c-Myc-mediated transcriptional repression and neoplastic transformation.The Journal of clinical investigation · 1996Article
- The major histocompatibility complex class II Ea promoter requires TFIID binding to an initiator sequence.Molecular and cellular biology · 1996Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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