ArticleOncogene1999
Transforming activity of EWS/FLI is not strictly dependent upon DNA-binding activity.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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.
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.
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Who cites it
38 citing papers in PubMed, 91 citations in OpenAlex.
- Heterogeneous Folding Intermediates Govern the Conformational Pathway of the RNA Recognition Motif Domain of the Ewing Sarcoma Protein.Biomolecules · 2025Article
- Molecular basis of EWS interdomain self-association and its role in condensate formation.Protein science : a publication of the Protein Society · 2025Article
- Phase separation of the oncogenic fusion protein EWS::FLI1 is modulated by its DNA-binding domain.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Insights into Molecular Diversity within the FUS/EWS/TAF15 Protein Family: Unraveling Phase Separation of the N-Terminal Low-Complexity Domain from RNA-Binding Protein EWS.Journal of the American Chemical Society · 2024Article
- Insights into Molecular Diversity within the FET Family: Unraveling Phase Separation of the N-Terminal Low Complexity Domain from RNA-Binding Protein EWS.bioRxiv : the preprint server for biology · 2023Article
- Biochemical and biophysical characterization of the nucleic acid binding properties of the RNA/DNA binding protein EWS.Biopolymers · 2023Article
- Comprehensive profiling of mRNA splicing indicates that GC content signals altered cassette exon inclusion in Ewing sarcoma.NAR cancer · 2022Article
- RNA-binding proteins of COSMIC importance in cancer.The Journal of clinical investigation · 2021Review
- Review
- Development of an Ewing sarcoma cell line with resistance to EWS‑FLI1 inhibitor YK‑4‑279.Molecular medicine reports · 2020Article
- Oncogenic fusion protein EWS-FLI1 is a network hub that regulates alternative splicing.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Structure-function based molecular relationships in Ewing's sarcoma.BioMed research international · 2015Review
- Anti-Epileptic Drug Targets Ewing Sarcoma.Journal of pharmaceutical sciences and pharmacology · 2014Article
- Tumor-specific retargeting of an oncogenic transcription factor chimera results in dysregulation of chromatin and transcription.Genome research · 2012Article
- The EWS/FLI Oncogene Drives Changes in Cellular Morphology, Adhesion, and Migration in Ewing Sarcoma.Genes & cancer · 2012Article
- Promiscuous partnerships in Ewing's sarcoma.Cancer genetics · 2011Review
- Article
- EWS/ETS proteins promote expression and regulate function of the homeodomain transcription factor BRN3A.Oncogene · 2010Article
- Ewing Sarcoma, an enigmatic malignancy of likely progenitor cell origin, driven by transcription factor oncogenic fusions.International journal of clinical and experimental pathology · 2010Review
- The TET family of proteins: functions and roles in disease.Journal of molecular cell biology · 2009Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In approximately 85% of Ewing sarcomas, chromosomal translocations give rise to the chimeric gene EWS/FLI, encoding the N-terminus of the RNA binding protein EWS fused to the DNA-binding domain of the ETS protein FLI-1. EWS/FLI is a stronger transcriptional activator than wild-type FLI-1, although both proteins bind to the same DNA sequences in vitro. In addition, EWS/FLI, but not FLI-1, is a transforming oncogene in NIH3T3 fibroblasts. EWS/FLI is thought to transform through its ability to deregulate the expression of target genes. We introduced several point mutations into the ETS domain of EWS/FLI that abolished DNA-binding activity. Although two of these mutations disrupted the transforming activity of EWS/FLI, one mutated protein containing a substitution of isoleucine 347 with glutamic acid (I347E) retained diminished transforming activity. In addition, EWS/FLI I347E did not activate expression of the endogenous EWS/FLI target gene manic fringe (MFNG). These studies demonstrate that a portion of the oncogenic activity of EWS/FLI is independent of FLI DNA-binding activity.
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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.