ArticleOncogene2004
The effects of Brn-3a on neuronal differentiation and apoptosis are differentially modulated by EWS and its oncogenic derivative EWS/Fli-1.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- EWSR1 prevents the induction of aneuploidy through direct regulation of Aurora B.Frontiers in cell and developmental biology · 2023Article
- EWSR1 regulates mitosis by dynamically influencing microtubule acetylation.Cell cycle (Georgetown, Tex.) · 2016Article
- Inactivation of EWS reduces PGC-1α protein stability and mitochondrial homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Uvrag targeting by Mir125a and Mir351 modulates autophagy associated with Ewsr1 deficiency.Autophagy · 2015Article
- The multifunctional protein fused in sarcoma (FUS) is a coactivator of microphthalmia-associated transcription factor (MITF).The Journal of biological chemistry · 2014Article
- Molecular detection and targeting of EWSR1 fusion transcripts in soft tissue tumors.Medical oncology (Northwood, London, England) · 2013Review
- Ewing sarcoma protein: a key player in human cancer.International journal of cell biology · 2013Review
- Ecteinascidin 743 interferes with the activity of EWS-FLI1 in Ewing sarcoma cells.Neoplasia (New York, N.Y.) · 2011Article
- Article
- EWS/ETS proteins promote expression and regulate function of the homeodomain transcription factor BRN3A.Oncogene · 2010Article
- AML1/ETO proteins control POU4F1/BRN3A expression and function in t(8;21) acute myeloid leukemia.Cancer research · 2010Article
- A simple technique for the prediction of interacting proteins reveals a direct Brn-3a-androgen receptor interaction.The Journal of biological chemistry · 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
- IGF1 is a common target gene of Ewing's sarcoma fusion proteins in mesenchymal progenitor cells.PloS one · 2008Article
- Ewing sarcoma protein ewsr1 maintains mitotic integrity and proneural cell survival in the zebrafish embryo.PloS one · 2007Article
- Ewing sarcoma gene EWS is essential for meiosis and B lymphocyte development.The Journal of clinical investigation · 2007Article
- Differential regulation of different human papilloma virus variants by the POU family transcription factor Brn-3a.Oncogene · 2006Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
Abstract
The Brn-3 family of POU (Pit-Oct-Unc) homeodomain transcription factors regulate differentiation of neuronal cell types. The transcriptional activator Brn-3a is expressed in Ewing's sarcomas, which also express characteristic chimaeric proteins as a consequence of fusion of the TET family gene EWS to one of several ETS genes. We have previously demonstrated a physical interaction between Brn-3a and EWS proteins, and show here that the C-terminal POU domain but not N-terminal activation domain of Brn-3a can interact in vitro with the RNA-binding domain of EWS. Likely due to POU domain homology, the related factor Brn-3b can also interact with EWS, but to a lesser extent than Brn-3a. Importantly, Brn-3a but not Brn-3b interacts in vitro with chimaeric EWS/Fli-1, EWS/ATF-1 and EWS/ERG proteins. Furthermore, overexpression of EWS/Fli-1 but not EWS or Fli-1 inhibits Brn-3a-associated growth arrest and neurite outgrowth in neuronal cells, and specifically inhibits Brn-3a-dependent activation of p21 and SNAP-25 transcription. In contrast, upregulation of Bcl-2 expression and inhibition of apoptosis by Brn-3a is antagonized more by EWS than by EWS/Fli-1. These data demonstrate that oncogenic rearrangement of EWS to produce EWS/Fli-1 may enhance the antiapoptotic effect of Brn-3a and inhibit its ability to promote neuronal differentiation.
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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.