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. 2013 Feb 28;8(2):e57545. doi: 10.1371/journal.pone.0057545

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© 2013 Gerhardt 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) Western blot analysis of E11.5 embryo and heart protein lysates. Actin serves as loading control. In Ftm-negative embryos (n = 3), there is more Gli3-190 protein than in wild-type littermates, but an equal amount of Gli3-83. The amount of Gli3-190 protein is higher in Ftm-deficient than in wild-type hearts (n = 12, respectively), while conversely, there is less Gli3-83 in Ftm ^−/− hearts indicating a processing defect in Ftm-negative hearts. (B, C) Graphical evaluation of the Gli3-190/Gli3-83 ratio in wild-type and Ftm-deficient embryos and hearts, respectively. (B) The ratio of Gli3-190/Gli3-83 is 2.64 fold elevated in Ftm-homozygous mutant embryos. (C) Gli3-190/Gli3-83 ratio is 10.94 fold increased in Ftm-negative hearts.