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. 1997 Jul 22;94(15):7909–7914. doi: 10.1073/pnas.94.15.7909

Figure 2.

Figure 2

Activation of RIP14 by TTNPB, RXR by LG1069, and both by tRA. (A) Cotransfected RIP14 plus RXR respond to both TTNPB and the RXR-specific agonist LG1069. JEG-3 cells were transfected as in Fig. 1 and treated with no ligand, 5 μM TTNPB, 1 μM LG1069, or 5 μM TTNPB plus 1 μM LG1069. (B) AF-2 regions deleted from RIP14 and RXRα. Amino acids 476–484 of RIP14 and 444–462 of RXRα were deleted to generate RIP14–Δ9C and RXR–Δ19C, respectively. The regions corresponding to the AF-2 motif (36) are identified in bold, and the regions deleted in each receptor are underlined. TRα is included for comparison. (C) AF-2 deletions demonstrate that RIP14 is activated by TTNPB, that RXR is activated by LG1069, and that both receptors respond to tRA. JEG-3 cells were transfected with the indicated expression vectors as in Fig. 1 and treated with either no ligand, 5 μM TTNPB, 10 μM tRA, or 100 nM LG1069.