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. 2014 Aug 5;9(8):e104338. doi: 10.1371/journal.pone.0104338

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© 2014 Chakraborty 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) Immunoblots of CaMKII and pCaMKII-T286 of heart homogenates from 10-day old Ryr2^+/+/AC3-C (WC) and/AC3-I (WI) and Ryr2^ADA/ADA/AC3-C (HC) and/AC3-I (HI) mice. Glyceraldehyde-3 phosphate dehydrogenase was the loading control. (B) Protein levels of CaMKII normalized to Ryr2^+/+/AC3-C. (C) pCaMKII/CaMKII on Thr-286. Data were obtained analyzing proteins from 4–6 hearts of each genotype and are the mean ± SEM of 15–16 (B) and 5–7 (C) determinations using two way ANOVA. None of the differences were significant.