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. Author manuscript; available in PMC: 2009 Apr 30.
Published in final edited form as: Mol Endocrinol. 2007 May 22;21(8):1924–1939. doi: 10.1210/me.2007-0035

Fig. 3. The Ability of MAPKKK Signaling to Inhibit the Core-pressor Interaction with TRα or RARα depends on both the Class and the Splice Form of the Corepressor.

Fig. 3

A, Certain corepressor splice variants are refractory, whereas others are sensitive to inhibition by MEKK1 signaling/ interaction assay with TRα. The mammalian TRα/corepressor two-hybrid assays in Fig. 1, C and D, were repeated in the absence or presence of a cotransfected, constitutively active MEKK1 construct. A GAL4DBD-SMRTα construct lacking SMRTα codons 1902 to 1994 was also included. “Relative-inhibition by MEKK1” represents the portion of the relative luciferase activity observed for each splice variant in the absence of MEKK1 signaling that is lost in response to MEKK1 signaling, e.g. 1.0 would represent a complete loss of interaction in response to MEKK1, whereas 0 would represent no inhibition. B, Certain corepressor splice variants are refractory, whereas others are sensitive to inhibition by MEKK1 signaling/interaction assay with RARα. The mammalian two-hybrid assays in Fig. 2, A and B, measuring the interaction of GAL4AD-RARα with the various GAL4DBD-corepressor constructs, was repeated in the absence or presence of a cotransfected, constitutively active MEKK1 construct. The overall experiments and analysis was as in A above.