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. 2014 Jun 19;3(3):e000976. doi: 10.1161/JAHA.114.000976

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© 2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Figure 7. — Has2 expression is regulated by Dnmt3b. A, MassArray showing increased Has2 enhancer methylation at E14.5 (n=2). B, RT‐qPCR showing decreased Has2 expression at E14.5 (n=3). C, RNA in situ hybridization showing that Has2 expression is predominantly in the atrioventricular canal (avc), with less expression in the myocardium (myo) at E11.5; and the expression is diminished by E14.5. mv/tv, mitral/tricuspid valve; ivs, interventricular septum. D, IHC showing Dnmt3b is predominantly expressed in AVC at E11.5. E, X‐gal staining showing the Nfatc1‐Cre mediated LacZ expression in the AVC at E11.5. F, RT‐qPCR showing that deletion of Dnmt3b resulted in increased Has2 expression at E11.5 and E14.5 (n=3). Error bars represent standard error. *Marks statistical significance (P<0.001, 2 factor ANOVA in [F]). ANOVA indicates analysis of variance; CKO, conditional knockout; IHC, immunohistochemistry; RT‐qPCR, quantitative real‐time polymerase chain reaction; WT, wild type.