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. Author manuscript; available in PMC: 2012 Jun 15.
Published in final edited form as: Gene. 2011 Feb 16;479(1-2):16–28. doi: 10.1016/j.gene.2011.02.002

Fig. 8.

Fig. 8

ERα physically associates with TCF-4. Fetal rat osteoblasts were transfected for 24 hours to express reporter plasmid 5XGAL4 in combination with expression plasmids encoding empty vector M driving the expression of GAL4DBD or vector M fused to full length ERα or the ERα fragments indicated (A), and/or empty vector MVN driving the expression of the herpes virus protein 16 transactivation domain or MVN fused to transcription factor TCF-4 lacking its β-catenin binding domain (TCFt) (B). The cells were treated vehicle (0) or 10 nM 17βE and reporter gene enzyme activity was measured after 24 hours. 17βE significantly increased reporter gene expression through 5XGAL4 and MVN-TCTt significantly enhanced ERα dependent gene expression in 17βE treated cells (C). ERα fragment AB significantly enhanced reporter gene expression through 5XGAL4 relative to empty vector M but was not further increased by 17βE or MVN-TCFt co-expression, whereas all ERα fragments retaining domain E were significantly activated by 17βE and further enhanced by MVN-TCFt co-expression (D); (* = P <0.05).