Supplementary Materials

Supplementary Materials for:

RhoA signaling in cardiomyocytes protects against stress-induced heart failure but facilitates cardiac fibrosis

Jessica Lauriol, Kimberly Keith, Fabrice Jaffré, Anthony Couvillon, Abdel Saci, Sanjeewa A. Goonasekera, Jason R. McCarthy, Chase W. Kessinger, Jianxun Wang, Qingen Ke, Peter M. Kang, Jeffery D. Molkentin, Christopher Carpenter, Maria I. Kontaridis*

*Corresponding author. E-mail: mkontari{at}bidmc.harvard.edu

This PDF file includes:

  • Fig. S1. Generation of RhoA floxed mice.
  • Fig. S2. Mice with cardiomyocyte-specific deletion of RhoA do not show an overt pathological phenotype.
  • Fig. S3. Mice with cardiomyocyte-specific deletion of RhoA develop pathological hypertrophy in response to TAC.
  • Fig. S4. Decreased RhoA expression in cardiomyocytes decreases the expression of fibrosis-related genes.
  • Table S1. Primer sequences.

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Citation: J. Lauriol, K. Keith, F. Jaffré, A. Couvillon, A. Saci, S. A.Goonasekera, J. R. McCarthy, C. W. Kessinger, J. Wang, Q. Ke, P. M. Kang, J. D. Molkentin, C. Carpenter, M. I. Kontaridis, RhoA signaling in cardiomyocytes protects against stress-induced heart failure but facilitates cardiac fibrosis. Sci. Signal. 7, ra100 (2014).

© 2014 American Association for the Advancement of Science