ArticleMolecular and cellular biology1995
An essential domain of the c-myc protein interacts with a nuclear factor that is also required for E1A-mediated transformation.
Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 64 citations in OpenAlex.
- Luminescence complementation technology for the identification of MYC:TRRAP inhibitors.Oncotarget · 2021Article
- Gene Transactivation and Transrepression in MYC-Driven Cancers.International journal of molecular sciences · 2021Review
- Formation of a structurally-stable conformation by the intrinsically disordered MYC:TRRAP complex.PloS one · 2019Article
- Premetazoan ancestry of the Myc-Max network.Molecular biology and evolution · 2011Article
- Point mutations in c-Myc uncouple neoplastic transformation from multiple other phenotypes in rat fibroblasts.PloS one · 2010Article
- Promotion of direct reprogramming by transformation-deficient Myc.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- RVB1/RVB2: running rings around molecular biology.Molecular cell · 2009Review
- Transcription profiling of lung adenocarcinomas of c-myc-transgenic mice: identification of the c-myc regulatory gene network.BMC systems biology · 2008Article
- Stimulation of Myc transactivation by the TATA binding protein in promoter-reporter assays.BMC biochemistry · 2005Article
- A global transcriptional regulatory role for c-Myc in Burkitt's lymphoma cells.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Article
- Quantitative proteomic analysis of Myc oncoprotein function.The EMBO journal · 2002Article
- TRRAP-dependent and TRRAP-independent transcriptional activation by Myc family oncoproteins.Molecular and cellular biology · 2002Article
- c-MYC overexpression in Ba/F3 cells simultaneously elicits genomic instability and apoptosis.Oncogene · 2002Article
- Article
- S-phase-specific expression of the Mad3 gene in proliferating and differentiating cells.The Biochemical journal · 2001Article
- Article
- Transforming ability of Gag-Myc fusion proteins correlates with Gag-Myc protein stability and transcriptional repression.Oncogene · 2001Article
- Myc is an essential negative regulator of platelet-derived growth factor beta receptor expression.Molecular and cellular biology · 2000Article
- Genetic dissection of c-myc apoptotic pathways.Oncogene · 2000Article
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5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell transformation by nuclear oncogenes such as c-myc presumably involves the transcriptional activation of a set of target genes that participate in the control of cell division. The function of a small evolutionarily conserved domain of the c-myc gene encompassing amino acids 129 to 145 was analyzed to explore the relationship between cell transformation and transcriptional activation. Deletion of this domain inactivated the c-myc oncogene for cell transformation while retaining the ability to activate transcription of either myc consensus binding sites or a GAL4-dependent promoter when the c-myc N-terminus was fused to the GAL4 DNA-binding domain. Point mutations that altered a conserved tryptophan (amino acid 136) within this domain had similar effects. Expression of the wt c-Myc N terminus (amino acids 1 to 262) as a GAL4 fusion was a dominant inhibitor of cell transformation by the c-myc oncogene, and this same domain also inhibited transformation by the adenovirus E1A gene. Surprisingly, deletion of amino acids 129 to 145 eliminated the dominant negative activity of GAL4-Myc on both c-myc and E1A transformation. Expression of the GAL4-Myc protein in Cos cells led to the formation of a specific complex between the Myc N terminus and a nuclear factor, and this complex was absent with the dl129-145 mutant. These results suggest that an essential domain of the c-Myc protein interacts with a specific nuclear factor that is also required for E1A transformation.
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