pubmed-article:8246959 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8246959 | lifeskim:mentions | umls-concept:C1533585 | lld:lifeskim |
pubmed-article:8246959 | lifeskim:mentions | umls-concept:C0029016 | lld:lifeskim |
pubmed-article:8246959 | lifeskim:mentions | umls-concept:C0553580 | lld:lifeskim |
pubmed-article:8246959 | lifeskim:mentions | umls-concept:C0808901 | lld:lifeskim |
pubmed-article:8246959 | lifeskim:mentions | umls-concept:C1336776 | lld:lifeskim |
pubmed-article:8246959 | lifeskim:mentions | umls-concept:C2700640 | lld:lifeskim |
pubmed-article:8246959 | pubmed:issue | 12 | lld:pubmed |
pubmed-article:8246959 | pubmed:dateCreated | 1994-1-3 | lld:pubmed |
pubmed-article:8246959 | pubmed:abstractText | EWS/FLI-1 is a chimeric protein formed by a tumor-specific 11;22 translocation found in both Ewing's sarcoma and primitive neuroectodermal tumor of childhood. EWS/FLI-1 has been shown to be a potent transforming gene, suggesting that it plays an important role in the genesis of these human tumors. We now demonstrate that EWS/FLI-1 has the characteristics of an aberrant transcription factor. Subcellular fractionation experiments localized the EWS/FLI-1 protein to the nucleus of primitive neuroectodermal tumor cells. EWS/FLI-1 specifically bound in vitro an ets-2 consensus sequence similarly to normal FLI-1. When coupled to a GAL4 DNA-binding domain, the amino-terminal EWS/FLI-1 region was a much more potent transcriptional activator than the corresponding amino-terminal domain of FLI-1. Finally, EWS/FLI-1 efficiently transformed NIH 3T3 cells, but FLI-1 did not. These data suggest that EWS/FLI-1, functioning as a transcription factor, leads to a phenotype dramatically different from that of cells expressing FLI-1. EWS/FLI-1 could disrupt normal growth and differentiation either by more efficiently activating FLI-1 target genes or by inappropriately modulating genes normally not responsive to FLI-1. | lld:pubmed |
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pubmed-article:8246959 | pubmed:language | eng | lld:pubmed |
pubmed-article:8246959 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8246959 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:8246959 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:8246959 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8246959 | pubmed:month | Dec | lld:pubmed |
pubmed-article:8246959 | pubmed:issn | 0270-7306 | lld:pubmed |
pubmed-article:8246959 | pubmed:author | pubmed-author:MayW AWA | lld:pubmed |
pubmed-article:8246959 | pubmed:author | pubmed-author:LewisB CBC | lld:pubmed |
pubmed-article:8246959 | pubmed:author | pubmed-author:DennyC TCT | lld:pubmed |
pubmed-article:8246959 | pubmed:author | pubmed-author:BraunB SBS | lld:pubmed |
pubmed-article:8246959 | pubmed:author | pubmed-author:LessnickS LSL | lld:pubmed |
pubmed-article:8246959 | pubmed:author | pubmed-author:HromasRR | lld:pubmed |
pubmed-article:8246959 | pubmed:author | pubmed-author:KlemszMM | lld:pubmed |
pubmed-article:8246959 | pubmed:author | pubmed-author:LunsfordL BLB | lld:pubmed |
pubmed-article:8246959 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8246959 | pubmed:volume | 13 | lld:pubmed |
pubmed-article:8246959 | pubmed:geneSymbol | EWS | lld:pubmed |
pubmed-article:8246959 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8246959 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8246959 | pubmed:pagination | 7393-8 | lld:pubmed |
pubmed-article:8246959 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:8246959 | pubmed:year | 1993 | lld:pubmed |
pubmed-article:8246959 | pubmed:articleTitle | The Ewing's sarcoma EWS/FLI-1 fusion gene encodes a more potent transcriptional activator and is a more powerful transforming gene than FLI-1. | lld:pubmed |
pubmed-article:8246959 | pubmed:affiliation | Department of Pediatrics, Gwynne Hazen Cherry Memorial Laboratories, University of California, Los Angeles. | lld:pubmed |