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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAMDBmTjxgc8sguHudMFSPrAw1jOGGEvxdakDqutrEV9Y#_6 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAMDBmTjxgc8sguHudMFSPrAw1jOGGEvxdakDqutrEV9Y#_5 http://www.w3.org/ns/prov#value In this study, we found that the transcriptional activity of human Erg (one of the Ets family-transcription factors) was repressed by several nuclear receptors, including human estrogen receptor ERalpha, nonsteroid receptors and orphan receptors. Conversely, Erg inhibited ERalpha-dependent transcription. These reciprocal functional interactions extended to other nuclear receptors such as thyroid hormone and retinoic acid receptors, as well as to Fli1, an ERG-related ETS factor. We confirmed mutual interference between FLI1 and either RARalpha or TRalpha1 into ROS cells and also observed such interactions between FLI1 and ERalpha, TRbeta1 and RXRalpha (data not shown). 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