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. Author manuscript; available in PMC: 2017 Jun 1.
Published in final edited form as: J Mol Endocrinol. 2016 Feb 9;56(3):273–290. doi: 10.1530/JME-15-0283

Figure 2.

Figure 2

MuRF1 inhibits TRα transcriptional activity following T3 treatment without affecting its steady-state levels. (A) TRE reporter assay results from Cos-7 cells co-transfected with luciferase plasmid containing TRE (or β-galactosidase control), and FLAG-TRα plasmid, transduced with AdMuRF1 (4 h), then treated with 16.6 nM T3 for 24 h (n = 3 independent experiments). Immunoblot verifying FLAG-TRα and myc-MuRF1 protein expression shown below graph. (B) Relative expression of TR transcriptionally regulated genes; HL-1 cells were transfected with AdMuRF1 (or AdGFP control) for 24 h and then treated with T3 for 30 min (C) Immunoblot of endogenous TR protein expression following MuRF1 knock-down (shMuRF1) or increased MuRF1 expression (AdMuRF1) in HL-1 cardiomyocytes (β-actin = loading control). Quantitative data shown in graphs below blots. Data are represented as mean ± S.E.M. (n = 3 independent experiments). A two-way ANOVA test was used to determine statistical significance. *Significance on the level of plasmid group. The F statistic and degrees of freedom (DF) were reported when dependence between groups was found to be a significant source of variation. Significance between groups is represented as #P < 0.05 as determined using a pairwise post-test; n.s. = not significant.