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. 2017 Oct 27;6(11):e007038. doi: 10.1161/JAHA.117.007038

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© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Arterial differentiation and maturation defects in Regulator of G protein signaling 6 (RGS6)^−/−/Ca²⁺/calmodulin‐dependent protein kinase II (CaMKII)^VV embryos. A, mRNA expression levels of endothelial precursors (fms related tyrosine kinase 1 [FLT1] and fetal liver kinase 1 [FLK1]), the vascular endothelial marker (VE‐cadherin), arterial markers (Ephrin B2, gap junction protein alpha 4, and gap junction protein alpha 5), and the venous marker (EphrinB4) were analyzed by quantitative polymerase chain reaction in E10.5 embryos and their yolk sacs. N=3, *P<0.001. B, Sm22 immunostaining of the dorsal aorta revealed a lack of smooth muscle recruitment in RGS6^−/−/CaMKII^VV embryos compared with RGS6^−/−/CaMKII^MM embryos. Scale bars=20 μm.