ArticleMolecular and cellular biology1990
An amino-terminal c-myc domain required for neoplastic transformation activates transcription.
Article in Molecular and cellular biology, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
176 citing papers in PubMed, 404 citations in OpenAlex.
- Mechanism of interaction between the transactivation domain of N-myc and the DNA-binding surface of TFIIIC5.Nucleic acids research · 2026Article
- Spatially-resolved Photoproximity Profiling of MYC Identifies a MYC-BAF Liability in Cancer Cells.bioRxiv : the preprint server for biology · 2025Article
- Aurora A binds to the transactivation domain of c-Myc and recognizes the phosphorylated N-terminal degron motif.The Biochemical journal · 2025Article
- Transcriptional activation and coactivator binding by yeast Ino2 and human proto-oncoprotein c-Myc.Current genetics · 2025Article
- DLGAP5 enhances bladder cancer chemoresistance by regulating glycolysis through MYC stabilization.Theranostics · 2025Article
- Roles of deubiquitinases in urologic cancers (Review).Oncology letters · 2024Review
- Review
- Exploring the dynamics and interactions of the N-myc transactivation domain through solution nuclear magnetic resonance spectroscopy.The Biochemical journal · 2024Article
- Missense Mutations in Myc Box I Influence Nucleocytoplasmic Transport to Promote Leukemogenesis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Isoform-Directed Control of c-Myc Functions: Understanding the Balance from Proliferation to Growth Arrest.International journal of molecular sciences · 2023Review
- BRD4 and MYC: power couple in transcription and disease.The FEBS journal · 2023Review
- Cancer Metabolism Historical Perspectives: A Chronicle of Controversies and Consensus.Cold Spring Harbor perspectives in medicine · 2023Article
- Deregulated Metabolic Pathways in Ovarian Cancer: Cause and Consequence.Metabolites · 2023Review
- Review
- MYC function and regulation in physiological perspective.Frontiers in cell and developmental biology · 2023Review
- Review
- Targeting the MDM2-p53 pathway in dedifferentiated liposarcoma.Frontiers in oncology · 2022Review
- Article
- Taking the Myc out of cancer: toward therapeutic strategies to directly inhibit c-Myc.Molecular cancer · 2021Review
- NSD3S stabilizes MYC through hindering its interaction with FBXW7.Journal of molecular cell biology · 2020Article
116 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 2 institutions in 1 country.
Funding
Abstract
The product of the c-myc proto-oncogene is a nuclear phosphoprotein whose normal cellular function has not yet been defined. c-Myc has a number of biochemical properties, however, that suggest that it may function as a potential regulator of gene transcription. Specifically, it is a nuclear DNA-binding protein with a short half-life, a high proline content, segments that are rich in glutamine and acidic residues, and a carboxyl-terminal oligomerization domain containing the leucine zipper and helix-loop-helix motifs that serve as oligomerization domains in known regulators of transcription, such as C/EBP, Jun, Fos, GCN4, MyoD, E12, and E47. In an effort to establish that c-Myc might regulate transcription in vivo, we sought to determine whether regions of the c-Myc protein could activate transcription in an in vitro system. We report here that fusion proteins in which segments of human c-Myc are linked to the DNA-binding domain of the yeast transcriptional activator GAL4 can activate transcription from a reporter gene linked to GAL4-binding sites. Three independent activation regions are located between amino acids 1 and 143, a region that has been shown to be required for neoplastic transformation of primary rat embryo cells in cooperation with a mutated ras gene. These results demonstrate that domains of the c-Myc protein can function to regulate transcription in a model system and suggest that alterations of Myc transcriptional regulatory function may lead to neoplastic transformation.
Indexed as
Identifiers
What OpenQuestion holds
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.