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Figure 3 | Nuclear Receptor

Figure 3

From: A conserved lysine in the estrogen receptor DNA binding domain regulates ligand activation profiles at AP-1 sites, possibly by controlling interactions with a modulating repressor

Figure 3

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.

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