Supplementary Materials

Supplementary Material for:

Inhibition of the Cardiomyocyte-Specific Kinase TNNI3K Limits Oxidative Stress, Injury, and Adverse Remodeling in the Ischemic Heart

Ronald J. Vagnozzi, Gregory J. Gatto Jr., Lara S. Kallander, Nicholas E. Hoffman, Karthik Mallilankaraman, Victoria L. T. Ballard, Brian G. Lawhorn, Patrick Stoy, Joanne Philp, Alan P. Graves, Yoshiro Naito, John J. Lepore, Erhe Gao, Muniswamy Madesh, Thomas Force*

*Corresponding author. E-mail: thomas.force@temple.edu

Published 16 October 2013, Sci. Transl. Med. 5, 207ra141 (2013)
DOI: 10.1126/scitranslmed.3006479

This PDF file includes:

  • Methods
    Fig. S1. TNNI3K is localized to the cardiomyocyte nucleus.
  • Fig. S2. Basal LV function, hemodynamics, and cardiac morphometry in Tg- TNNI3K and Tg-KI TNNI3K mice.
  • Fig. S3. Post-I/R activation status of ERK1/2, JNK, and Akt in TNNI3K transgenic mice.
  • Fig. S4. Basal p38 MAPK activation status in TNNI3K transgenic mice.
  • Fig. S5. ERK1/2, JNK, and Akt activation status after TNNI3K overexpression in NRVMs.
  • Fig. S6. TNNI3K-induced cell death is blunted by selective knockdown of p38α in NRVMs.
  • Fig. S7. GSK854 rescues the effect of TNNI3K overexpression on ROS generation in NRVMs.
  • Fig. S8. Tnni3k deletion does not alter adverse LV remodeling after permanent occlusion MI.
  • Table S1. LV function and cardiac morphometry in inducible cardiomyocytespecific Tnni3k-KO mice.
  • Table S2. Selectivity profiles of small-molecule TNNI3K inhibitors.

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