Figure 2.

Differential role of LXD motifs in actions of ER (A), PR (B), RAR (C), or TR (D) receptors. In each case, ligands were added at 10⁻⁶ m, and reporters were under control of the appropriate response element (Torchia et al. 1997). (ERE) Estrogen-responds element; (PRE) progesterone-response element; (RARE) retinoic acid-response element; (TRE) thyroid hormone-response element. Rat-1 cells were microinjected with anti-NCoA-1/SRC-1 IgG and the CMV-expression vectors encoding the indicated proteins (Torchia et al. 1997). In addition to the mutations in leucine residues +4 and +5 of each motif, a deletion of 30 amino acids between LXD2 and LXD3 (LXD2S3mut) were created, leaving the 10 amino acids immediately flanking the LXD intact. Ligands were retinoic acid (RA), triiodothyronine (T3), 17β-estradiol (E₂), or progesterone (Prog). Where indicated, receptors were also expressed; similar results were obtained in at least three independent experiments with >300 cells microinjected for each data point.