| The high levels of DAX1 found in Ewing tumors and its potent transcriptional repressor activity suggest that the oncogenic effect of EWS/FLI1 may be mediated, at least in part, by the up-regulation of DAX1 expression. | None |
| The orphan nuclear receptor DAX1 is up-regulated by the EWS/FLI1 oncoprotein and is highly expressed in Ewing tumors. | None |
| Oncoprotein EWS-FLI1 activity is enhanced by RNA helicase A. | None |
| Identification and characterization of the nuclear localization/retention signal in the EWS proto-oncoprotein. | None |
| EWS/FLI-1 oncoprotein subtypes impose different requirements for transformation and metastatic activity in a murine model. | None |
| The EWS/FLI1 oncogenic transcription factor deregulates GLI1. | None |
| DAX1, a direct target of EWS/FLI1 oncoprotein, is a principal regulator of cell-cycle progression in Ewing s tumor cells. | None |
| Mutation in the DNA-binding domain of the EWS-Oct-4 oncogene results in dominant negative activity that interferes with EWS-Oct-4-mediated transactivation. | None |
| GLI1 is a direct transcriptional target of EWS-FLI1 oncoprotein. | None |
| In vitro activity of the EWS oncogene transcriptional activation domain. | None |
| The oncogenic EWS-FLI1 protein binds in vivo GGAA microsatellite sequences with potential transcriptional activation function. | None |
| The EWS/FLI1 oncogenic protein inhibits expression of the Wnt inhibitor DICKKOPF-1 gene and antagonizes beta-catenin/TCF-mediated transcription. | None |
| EWS-Oct-4B, an alternative EWS-Oct-4 fusion gene, is a potent oncogene linked to human epithelial tumours. | None |
| EWS/FLI1 oncogene activates caspase 3 transcription and triggers apoptosis in vivo. | None |
| Oncogenic fusion protein EWS/FLI1 down-regulates gene expression by both transcriptional and posttranscriptional mechanisms. | None |
| Identification of an inhibitor of the EWS-FLI1 oncogenic transcription factor by high-throughput screening. | None |
| Novel peptide binds EWS-FLI1 and reduces the oncogenic potential in Ewing tumors. | None |
| Single enantiomer of YK-4-279 demonstrates specificity in targeting the oncogene EWS-FLI1. | None |
| Results show that EWSR1/FLI1 binding independent of E2F3 is predominantly associated with repressed differentiation genes. Thus, EWSR1/FLI1 appears to promote oncogenesis by simultaneously promoting cell proliferation and perturbing differentiation. | None |
| A conserved N-terminal motif is required for complex formation between FUS, EWSR1, TAF15 and their oncogenic fusion proteins. | None |