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. 2016 May 31;113(24):E3451–E3460. doi: 10.1073/pnas.1506113113

Fig. 2.

Fig. 2.

TRα and TRβ domains involved in repression of TGF-β induced transcription by T3. (A) Reporter assays in Mv1Lu cells transfected with a noncoding vector or with vectors encoding WT and mutant TRα. Luciferase activity was measured in cells incubated with T3 for 36 h and with TGF-β for the last 5 h. Results are expressed relative to the untreated cells transfected with an empty vector. (B) Scheme of TRα showing the position of the mutations. AF-2, ligand-dependent transcriptional activation function. (C) Western blot of TRα in untreated and T3-treated cells transfected with the different mutants. The arrow indicates the mobility of the TRα LBD. ERK2 was used as a loading control. (D) Luciferase activity in cells transfected with the TRβ mutants indicated and treated as in A. (E) Scheme of the mutations of TRβ used. (F) Expression of TRβ mutants in transfected cells. All data are mean ± SD (n = 3). Significance of ANOVA posttest (Bonferroni) of cells treated in the absence and presence of T3 is indicated. (G) ChIP assays performed with control IgG and anti-TRα or anti-TRβ antibodies in GH4C1 cells transfected with an empty plasmid (−) or with expression vectors for the indicated receptors. Precipitated DNA was examined by quantitative RT-PCR with primers specific for the SBE-containing region (−1,300/−1,042) of the Id1 promoter.