pubmed-article:15917470 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15917470 | lifeskim:mentions | umls-concept:C0553580 | lld:lifeskim |
pubmed-article:15917470 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
pubmed-article:15917470 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
pubmed-article:15917470 | lifeskim:mentions | umls-concept:C1882263 | lld:lifeskim |
pubmed-article:15917470 | lifeskim:mentions | umls-concept:C1948023 | lld:lifeskim |
pubmed-article:15917470 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:15917470 | pubmed:dateCreated | 2005-5-26 | lld:pubmed |
pubmed-article:15917470 | pubmed:abstractText | The Oct-4 gene encodes a transcription factor that is expressed in embryonic stem (ES) cells and germ cells. Oct-4 is known to function as a transcriptional activator of genes involved in maintaining an undifferentiated totipotent state and possibly in preventing expression of genes activated during differentiation. In addition, it is a putative proto-oncogene and a critical player in the genesis of human testicular germ cell tumors. Although much effort has gone toward characterizing Oct-4, there is still little known about the molecular mechanisms and the proteins that regulate Oct-4 function. To identify cofactors that control Oct-4 function in vivo, we used a recently developed bacterial two-hybrid screening system and isolated a novel ES cell-derived cDNA encoding Ewing's sarcoma protein (EWS). EWS is a proto-oncogene and putative RNA-binding protein involved in human cancers. By using glutathione-S-transferase (GST) pull-down assays, we were able to confirm the interaction between Oct-4 and EWS in vitro, and moreover, coimmunoprecipitation and colocalization studies have shown that these proteins also associate in vivo. We have mapped the EWS-interacting region to the POU domain of Oct-4. In addition, three independent sites on EWS are involved in binding to Oct-4. In this study, we report that Oct-4 and EWS are coexpressed in the pluripotent mouse and human ES cells. Consistent with its ability to bind to and colocalize with Oct-4, ectopic expression of EWS enhances the transactivation ability of Oct-4. Moreover, a chimeric protein generated by fusion of EWS (1-295) to the GAL4 DNA-binding domain significantly increases promoter activity of a reporter containing GAL4 DNA-binding sites, suggesting the presence of a strong activation domain within EWS. Taken together, our results suggest that Oct-4-mediated transactivation is stimulated by EWS. | lld:pubmed |
pubmed-article:15917470 | pubmed:language | eng | lld:pubmed |
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pubmed-article:15917470 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:15917470 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15917470 | pubmed:issn | 1066-5099 | lld:pubmed |
pubmed-article:15917470 | pubmed:author | pubmed-author:HanYong-MahnY... | lld:pubmed |
pubmed-article:15917470 | pubmed:author | pubmed-author:KimJunghoJ | lld:pubmed |
pubmed-article:15917470 | pubmed:author | pubmed-author:RheeByung... | lld:pubmed |
pubmed-article:15917470 | pubmed:author | pubmed-author:LeeJungwoonJ | lld:pubmed |
pubmed-article:15917470 | pubmed:author | pubmed-author:BaeGab-YongGY | lld:pubmed |
pubmed-article:15917470 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15917470 | pubmed:volume | 23 | lld:pubmed |
pubmed-article:15917470 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15917470 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15917470 | pubmed:pagination | 738-51 | lld:pubmed |
pubmed-article:15917470 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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pubmed-article:15917470 | pubmed:articleTitle | Stimulation of Oct-4 activity by Ewing's sarcoma protein. | lld:pubmed |
pubmed-article:15917470 | pubmed:affiliation | Laboratory of Molecular and Cellular Biology, Department of Life Science, Sogang University, Seoul 121-742, Korea. | lld:pubmed |
pubmed-article:15917470 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15917470 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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