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. 2015 Aug 17;112(35):E4884–E4893. doi: 10.1073/pnas.1512655112

Fig. 7.

Fig. 7.

miR-196 has the potential to regulate Wnt signaling by both direct and indirect mechanisms. (A) WISH analysis confirms increased Dkk1 in 196a1−/− ;196a2−/− E9.5 embryos relative to 196a1−/+;196a2−/+ (n = 2/2 for each genotype). (B) In vitro luciferase assay confirms sequence-specific regulation of Dkk1 by miR-196 . Renilla luciferase intensity values have been normalized to their respective Firefly values (RLU). Controls (WT 3′ UTR construct without miR-196b) were set to 1. MUT, mutated 3′ UTR construct destroying miR-196 binding site. (C) Luciferase assay measuring Wnt/β-catenin activity after overexpression of BATLuc together with CMV-Renilla and either control, Hoxb1, Hoxa5, Hoxa7, Hoxb7, Hoxb8, or Hoxc8; n = 4–9 samples per gene assessed. Firefly luciferase intensity values have been normalized to their respective Renilla values (RLU). Control values were set to 1. In B and C, error bars represent SD. Reported P values are from the Student t test: *P 0.05, **P < 0.005, ***P < 0.0005, and ****P < 0.0001.