Nature Medicine
11, 409 - 417 (2005)
Published online: 27 March 2005; | doi:10.1038/nm1215
Calmodulin kinase II inhibition protects against structural heart diseaseRong Zhang, Michelle S C Khoo, Yuejin Wu, Yingbo Yang, Chad E Grueter, Gemin Ni, Edward E Price Jr., William Thiel, Silvia Guatimosim, Long-Sheng Song, Ernest C Madu, Anisha N Shah, Tatiana A Vishnivetskaya, James B Atkinson, Vsevolod V Gurevich, Guy Salama, W J Lederer, Roger J Colbran
& Mark E AndersonSupplementary Fig. 1 (pdf 52K)
Similar heart weights (wt) and left ventricular (LV) chamber dimensions in AC3-I(I), wild type (WT) and
AC3-C (C) hearts. Supplementary Fig. 2 (pdf 94K)
Similar protein phosphatase expression in AC3-I, WT and AC3-C hearts. Supplementary Fig. 3 (pdf 44K)
Quantification of surgical myocardial infarctions. Supplementary Fig. 4 (pdf 86K)
Quantification of interventricular septal thickness after myocardial infarction surgery. Supplementary Fig. 5 (pdf 127K)
Heart rates in wild type mice 24 hours after injection with KN-93 or KN-92, at baseline or up to three weeks
after myocardial infarction. Supplementary Fig. 6 (pdf 148K)
Excitation-contraction coupling protein expression in AC3-I, AC3-C and wild type hearts. Supplementary Fig. 7 (pdf 179K)
Ryanodine receptor Ca2+ spark properties are not different between AC3-I and AC3-C
cardiomyocytes. Supplementary Methods (pdf 46K)
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