ERαK206A super-stimulation requires activation functions. (A) Truncation of AF-1 abolishes Tam response to ERα.K206A at AP-1 sites in MDA-MB-453 cells, which support AF-1 activity. (B) In HeLa cells, mutation of AF-2, also in the ERα.K206A background, abrogates K206A activity. Cells were transfected with ERs bearing K206A mutants in the context of full-length receptor, or the ERα DBD-LBD truncation lacking the NTD, which contains AF-1. (C) HeLa cells were transfected with ERα.DBD-LBD or its K206A equivalent, or a VP16-DBD-LBD fusion or its K206A equivalent. Note that E2, but not Tam, responses are amplified by the K206A mutation in the context of the DBD-LBD truncation but E2 and Tam responses are amplified by the K206A mutation in the context of the VP16-DBD-LBD fusion. Results of a representative experiment are shown.
Uht et al. Nuclear Receptor 2004 2:2 doi:10.1186/1478-1336-2-2