ArticleMolecular and cellular biology1993
B-myc inhibits neoplastic transformation and transcriptional activation by c-myc.
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 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 47 citations in OpenAlex.
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- Impairment of liver regeneration by the histone deacetylase inhibitor valproic acid in mice.Journal of Zhejiang University. Science. B · 2012Article
- Tripartite motif 24 (Trim24/Tif1α) tumor suppressor protein is a novel negative regulator of interferon (IFN)/signal transducers and activators of transcription (STAT) signaling pathway acting through retinoic acid receptor α (Rarα) inhibition.The Journal of biological chemistry · 2011Article
- Gene expression profiles in primary pancreatic tumors and metastatic lesions of Ela-c-myc transgenic mice.Molecular cancer · 2008Article
- B-Myc is preferentially expressed in hormonally-controlled tissues and inhibits cellular proliferation.Oncogene · 2000Article
- The Myc oncoprotein: a critical evaluation of transactivation and target gene regulation.Oncogene · 1999Review
- Molecular weight abnormalities of the CTCF transcription factor: CTCF migrates aberrantly in SDS-PAGE and the size of the expressed protein is affected by the UTRs and sequences within the coding region of the CTCF gene.Nucleic acids research · 1997Article
- Structure of pp32, an acidic nuclear protein which inhibits oncogene-induced formation of transformed foci.Molecular biology of the cell · 1996Article
- Transformation by the Bmi-1 oncoprotein correlates with its subnuclear localization but not its transcriptional suppression activity.Molecular and cellular biology · 1996Article
- Myc oncogenes: the enigmatic family.The Biochemical journal · 1996Review
- A link between increased transforming activity of lymphoma-derived MYC mutant alleles, their defective regulation by p107, and altered phosphorylation of the c-Myc transactivation domain.Molecular and cellular biology · 1995Article
- An essential domain of the c-myc protein interacts with a nuclear factor that is also required for E1A-mediated transformation.Molecular and cellular biology · 1995Article
- Hierarchical phosphorylation at N-terminal transformation-sensitive sites in c-Myc protein is regulated by mitogens and in mitosis.Molecular and cellular biology · 1994Article
- The c-Myc protein induces cell cycle progression and apoptosis through dimerization with Max.The EMBO journal · 1993Article
- The HMGA1-COX-2 axis: a key molecular pathway and potential target in pancreatic adenocarcinoma.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
B-myc is a recently described myc gene whose product has not been functionally characterized. The predicted product of B-myc is a 168-amino-acid protein with extensive homology to the c-Myc amino-terminal region, previously shown to contain a transcriptional activation domain. We hypothesized that B-Myc might also function in transcriptional regulation, although its role in regulating gene expression is predicted to be unique, because B-Myc lacks the specific DNA-binding motif found in other Myc proteins. To determine whether B-Myc could interact with the transcriptional machinery, we studied the transcriptional activation properties of a chimeric protein containing B-Myc sequences fused to the DNA-binding domain of the yeast transcriptional activator GAL4 (GAL4-B-Myc). We found that GAL4-B-Myc strongly activated expression of a GAL4-regulated reporter gene in mammalian cells. In addition, full-length B-Myc was able to inhibit or squelch reporter gene activation by a GAL4 chimeric protein containing the c-Myc transcriptional activation domain. We also observed that B-Myc dramatically inhibited the neoplastic cotransforming activity of c-Myc and activated Ras in rat embryo cells. Because B-Myc inhibits both neoplastic transformation and transcriptional activation by c-Myc, we suggest that the transforming activity of c-Myc is related to its ability to regulate transcription. Whether B-Myc functions biologically to squelch transcription and/or to regulate transcription through a specific DNA-binding protein remains unestablished.
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Registered trials
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.