ArticleMolecular and cellular biology1993
Oncogenic truncation of the first repeat of c-Myb decreases DNA binding in vitro and in vivo.
Article in Molecular and cellular biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 75 citations in OpenAlex.
- Structural Analysis of the SANT/Myb Domain of FLASH and YARP Proteins and Their Complex with the C-Terminal Fragment of NPAT by NMR Spectroscopy and Computer Simulations.International journal of molecular sciences · 2020Article
- Article
- Long-read single-molecule maps of the functional methylome.Genome research · 2019Article
- Situational awareness: regulation of the myb transcription factor in differentiation, the cell cycle and oncogenesis.Cancers · 2014Review
- Animal-specific C-terminal domain links myeloblastosis oncoprotein (Myb) to an ancient repressor complex.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Myb proteins: angels and demons in normal and transformed cells.Frontiers in bioscience (Landmark edition) · 2011Review
- The C-MYB story--is it definitive?Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- A conserved acidic patch in the Myb domain is required for activation of an endogenous target gene and for chromatin binding.Molecular cancer · 2008Article
- Myb proteins inhibit fibroblast transformation by v-Rel.Molecular cancer · 2006Article
- Oncogenic mutations cause dramatic, qualitative changes in the transcriptional activity of c-Myb.Oncogene · 2006Article
- Wnt-1 signal induces phosphorylation and degradation of c-Myb protein via TAK1, HIPK2, and NLK.Genes & development · 2004Article
- Alterations of the MDV oncogenic regions in an MDV transformed lymphoblastoid cell line.Molecular pathology : MP · 2002Article
- Identification and characterization of the Myb-inducible promoter of the chicken adenosine receptor 2B gene.Oncogene · 2002Article
- Tumorigenic N-terminal deletions of c-Myb modulate DNA binding, transactivation, and cooperativity with C/EBP.Oncogene · 2001Article
- BS69, an adenovirus E1A-associated protein, inhibits the transcriptional activity of c-Myb.Oncogene · 2001Article
- Functional analysis of carboxy-terminal deletion mutants of c-Myb.Journal of virology · 1999Article
- Transcriptional regulation by the carboxyl terminus of c-Myb depends upon both the Myb DNA-binding domain and the DNA recognition site.Oncogene · 1999Article
- Transformation by v-Myb.Oncogene · 1999Review
- Overexpression of an alternatively spliced form of c-Myb results in increases in transactivation and transforms avian myelomonoblasts.Journal of virology · 1998Article
- D-type cyclins repress transcriptional activation by the v-Myb but not the c-Myb DNA-binding domain.The EMBO journal · 1998Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Oncogenic activation of c-Myb in both avian and murine systems often involves N-terminal truncation. In particular, the first of three DNA-binding repeats in c-Myb has been largely deleted during the genesis of the v-myb oncogenes of avian myeloblastosis virus and E26 avian leukemia virus. This finding suggests that the first DNA-binding repeat may have an important role in cell growth control. We demonstrate that truncation of the first DNA-binding repeat of c-Myb is sufficient for myeloid transformation in culture, but deletion of the N-terminal phosphorylation site and adjacent acidic region is not. Truncation of the first repeat decreases the ability of a Myb-VP16 fusion protein to trans activate the promoter of a Myb-inducible gene (mim-1) involved in differentiation. Moreover, truncation of the first repeat decreases the ability of the Myb protein to bind DNA both in vivo and in vitro. These results suggest that N-terminal mutants of c-Myb may transform by regulating only a subset of those genes normally regulated by c-Myb.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.