ArticleMolecular and cellular biology1997
Identification of downstream-initiated c-Myc proteins which are dominant-negative inhibitors of transactivation by full-length c-Myc proteins.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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
62 citing papers in PubMed, 135 citations in OpenAlex.
- Prognostic relevance of c-MYC gene amplification and polysomy for chromosome 8 in suboptimally-resected, advanced stage epithelial ovarian cancers: a Gynecologic Oncology Group study.Gynecologic oncology · 2009Trial
- Pluripotency genes of mammals: a network at work.Frontiers in bioengineering and biotechnology · 2025Review
- Exploring the dynamics and interactions of the N-myc transactivation domain through solution nuclear magnetic resonance spectroscopy.The Biochemical journal · 2024Article
- Ribosome stalling duringPNAS nexus · 2024Article
- Isoform-Directed Control of c-Myc Functions: Understanding the Balance from Proliferation to Growth Arrest.International journal of molecular sciences · 2023Review
- AlternativeBiomolecules · 2022Article
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- Nesprin-2 Interacts with Condensin Component SMC2.International journal of cell biology · 2017Article
- Two isoforms of TALDO1 generated by alternative translational initiation show differential nucleocytoplasmic distribution to regulate the global metabolic network.Scientific reports · 2016Article
- Distribution of the c-MYC gene product in colorectal neoplasia.Histopathology · 2016Article
- High throughput screening identifies modulators of histone deacetylase inhibitors.BMC genomics · 2014Article
- MYC cofactors: molecular switches controlling diverse biological outcomes.Cold Spring Harbor perspectives in medicine · 2014Review
- MYC chromosomal aberration in differential diagnosis between Burkitt and other aggressive lymphomas.Infectious agents and cancer · 2013Article
- Nucleophosmin is essential for c-Myc nucleolar localization and c-Myc-mediated rDNA transcription.Oncogene · 2013Article
- Domain-specific c-Myc ubiquitylation controls c-Myc transcriptional and apoptotic activity.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- MYC on the path to cancer.Cell · 2012Review
- Two independent mechanisms promote expression of an N-terminal truncated USP18 isoform with higher DeISGylation activity in the nucleus.The Journal of biological chemistry · 2012Article
- Expression of Caytaxin protein in Cayman Ataxia mouse models correlates with phenotype severity.PloS one · 2012Article
- Premetazoan ancestry of the Myc-Max network.Molecular biology and evolution · 2011Article
2 more citing papers are in PubMed but not listed here.
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 1 institution in 1 country.
Funding
Abstract
The c-myc gene has been implicated in multiple cellular processes including proliferation, differentiation, and apoptosis. In addition to the full-length c-Myc 1 and 2 proteins, we have found that human, murine, and avian cells express smaller c-Myc proteins arising from translational initiation at conserved downstream AUG codons. These c-Myc short (c-Myc S) proteins lack most of the N-terminal transactivation domain but retain the C-terminal protein dimerization and DNA binding domains. As with full-length c-Myc proteins, the c-Myc S proteins appear to be localized to the nucleus, are relatively unstable, and are phosphorylated. Significant levels of c-Myc S, often approaching the levels of full-length c-Myc, are transiently observed during the rapid growth phase of several different types of cells. Optimization of the upstream initiation codons resulted in greatly reduced synthesis of the c-Myc S proteins, suggesting that a "leaky scanning" mechanism leads to the translation of these proteins. In some hematopoietic tumor cell lines having altered c-myc genes, the c-Myc S proteins are constitutively expressed at levels equivalent to that of full-length c-Myc. As predicted, the c-Myc S proteins are unable to activate transcription and inhibited transactivation by full-length c-Myc proteins, suggesting a dominant-negative inhibitory function. While these transcriptional inhibitors would not be expected to function as full-length c-Myc, the occurrence of tumors which express constitutive high levels of c-Myc S and their transient synthesis during rapid cell growth suggest that these proteins do not interfere with the growth-promoting functions of full-length c-Myc.
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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.