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. 2016 Jun 13;6:27746. doi: 10.1038/srep27746

Figure 4. nTRIP6 represses MEF2C transcriptional activity.

Figure 4

(a) C2C12 cells were transfected with either an siRNA targeting Trip6 mRNA or a control siRNA (Co), and 24 h later with a MEF2-dependent reporter gene together with an expression vector for β-galactosidase, and with either an expression vector for MEF2C (+) or an empty vector (−). Normalised luciferase activities are plotted relative to the control siRNA, empty vector transfected cells (mean ± SD of three independent experiments; *P < 0.05). (b) C2C12 cells were co-transfected with the MEF2-dependent reporter gene, the expression vector for β-galactosidase, either the expression vector for MEF2C (+) or the empty vector (−), together with either a control empty vector (V) or increasing amounts of an expression vector for nTRIP6, for nTRIP6 lacking the interaction domain 1 (nTRIP6ΔID1) or nTRIP6 lacking the interaction domain 2 (nTRIP6ΔID2). (c) C2C12 cells were co-transfected with the MEF2-dependent reporter gene, the expression vector for β-galactosidase, either the expression vector for MEF2C (+) or the empty vector (−), together with either a control empty vector (V), the mCherry-NLS fusion of either the ID1 peptide, its scrambled version (ID1c), the ID2 peptide or its scrambled version (ID2c). (b,c) Normalised luciferase activities are plotted relative to the empty vector control (mean ± SD of three independent experiments; *P < 0.05).