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. Author manuscript; available in PMC: 2018 Jun 2.
Published in final edited form as: Stem Cells. 2016 Sep 20;35(2):351–361. doi: 10.1002/stem.2484

Figure 5. YAP inhibited myocardin transcription by preventing NKX2.5 binding to myocardin promoter.

Figure 5

(A): Expression of myocardin in Vector control and YAP overexpressed group by RT-qPCR. (B): Expression of myocardin in scramble control and shYAP+shTAZ knockdown group by RT-qPCR. (C): Schematic of designs of luciferase reporters. (D): Luciferase activity of MYOCD-promoter WT by different dose of pCDNA-YAP in PAC1 cells. (E): Luciferase activity of MYOCD-promoter WT and NKE mut between pCDNA control and pCDNA-YAP in PAC1 cells. (F): Chip-PCR assay between Vector control and YAP overexpressed groups in PAC1 cells. (G): Co-IP assay in HEK 293 cells by overexpressing YAP-Myc and Nkx2.5 as indicated. Results were shown as average ± SEM and statistic analyzed with unpaired t-test.*p<0.05, **p<0.005, ***p<0.001, ns: no significance. WT: wild-type; NKE: NKX2.5 binding element; IP: immunoprecipitation; IB: immunoblot. M: molecular mass markers.