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. 2017 Jan 13;2(1):18–26. doi: 10.1016/j.ncrna.2016.12.002

Fig. 4.

Fig. 4

Improved cardiac function after pharmacological inhibition of miRNA-199b involves CnA/NFAT signaling. (a,b) Real-time PCR analysis of transcript abundance of (a) rcan1-4 and (b) dyrk1a in WT or miR-199b transgenic (TG) murine hearts after subjection to 4 weeks of sham or MI. (c) Western blot analysis of endogenous Dyrk1a and αTubulin in WT or miR-199b transgenic (TG) murine hearts after subjection to 4 weeks of sham or MI. (d) Quantification of αTubulin-corrected Dyrk1A western blot signals from (c). (e,f) Real-time PCR analysis of transcript abundance of (e) rcan1-4 and (f) dyrk1a in hearts from mice subjected to sham or MI, and treated either with antagomir-control or antagomir-199b. (g) Western blot analysis of endogenous Dyrk1a and αTubulin in murine hearts subjected to sham or MI, and treated either with antagomir-control or antagomir-199b. (h) Quantification of αTubulin-corrected Dyrk1A western blot signals from (g). n = 5–9 *P < 0.05 (mean ± s.e.m.).