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. 2014 Oct 9;9(10):e109493. doi: 10.1371/journal.pone.0109493

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© 2014 He et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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(A, B) Staining of BRDU shows reduced cardiomyocytes (CMs) proliferation in E13.5 BAF200 mutant hearts compared with littermate controls. *P<0.05. (C) phospho-histone H3 staining shows reduced proliferation in BAF200 mutant compact myocardium. (D) Expression of p57kip2, a cyclin-dependent kinase inhibitor, is increased in mutant hearts. (E) No significant apoptosis was detected in mutant and control embryos. (F, G) Expression of chamber-specific markers MYL2 and MYL7 was unchanged in BAF200-deficient hearts. (H, I) Expression of cardiac transcription factors GATA4 and Nkx2-5 were not significantly changed in BAF200 mutants. White bar = 100 um.