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. Author manuscript; available in PMC: 2011 Jun 6.
Published in final edited form as: J Cell Physiol. 2011 Apr;226(4):1035–1043. doi: 10.1002/jcp.22422

Fig. 4.

Fig. 4

MicroRNA-26a controls the activity of a TGF-β-activated SMAD reporter element. HEK-293 cells were dual-transfected with firefly luciferase SMAD reporter/constitutively expressing Renilla luciferase and either miRNA-26a antagomiR or pre-miR precursor, and treated with TGF-β. As expected, TGF-β treatment increased transcription of the SMAD-responsive TREs (SMAD/TGFβ), *P < 0.05 versus untreated reporter (SMAD). Addition of pre-miRNA-26a (SMAD/TGFβ/pre-26a) caused a significant drop in signaling compared with TGF-β-treated cells, while miRNA-26a antagomiR (SMAD/TGFβ/anti-26a) led to a significant activity increase, **P < 0.05.