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Figure 7 | Nuclear Receptor

Figure 7

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 7

TRα.K72 behaves similarly to ERα.K206A. (A) The K72 mutation eliminates unliganded and enhances liganded stimulation by TRα. HeLa cells were transfected as above using TRα and TRα.K72A, and then treated with 100 nM T3. (B) The K72A mutation abrogates unliganded TRα's ability to titrate a repressive function. The experiment was performed as in Fig. 6, except that cells were transfected with TRα (5 ug) and treated with 100 nM T3 instead of ER and ER ligands, respectively. (C) The K72A mutation enhances TRα's ability to inhibit transcription from classic thyroid response elements (TREs). Cells were transfected with 1 ug TRα and 2 ug TRE2-LUC reporter.

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