Joachim P Schmitt

Summary

Country: Germany

Publications

  1. ncbi Alterations of phospholamban function can exhibit cardiotoxic effects independent of excessive sarcoplasmic reticulum Ca2+-ATPase inhibition
    Joachim P Schmitt
    Institute of Pharmacology and Toxicology, University of Wurzburg, Wurzburg, Germany
    Circulation 119:436-44. 2009
  2. ncbi A new type of ERK1/2 autophosphorylation causes cardiac hypertrophy
    Kristina Lorenz
    Institute of Pharmacology and Toxicology, University of Wurzburg, Versbacher Strasse 9, Wurzburg, Germany
    Nat Med 15:75-83. 2009
  3. ncbi Cardiac hypertrophy: targeting Raf/MEK/ERK1/2-signaling
    Kristina Lorenz
    Institute of Pharmacology and Toxicology, University of Wurzburg, Versbacher Strasse 9, 97078 Wurzburg, Germany
    Int J Biochem Cell Biol 41:2351-5. 2009

Detail Information

Publications3

  1. ncbi Alterations of phospholamban function can exhibit cardiotoxic effects independent of excessive sarcoplasmic reticulum Ca2+-ATPase inhibition
    Joachim P Schmitt
    Institute of Pharmacology and Toxicology, University of Wurzburg, Wurzburg, Germany
    Circulation 119:436-44. 2009
    ..Here, we investigated whether PLN exhibits cardiotoxic effects via mechanisms other than chronic inhibition of SERCA2a by studying a PLN mutant, PLN(R9C), that triggers cardiac failure in humans and mice...
  2. ncbi A new type of ERK1/2 autophosphorylation causes cardiac hypertrophy
    Kristina Lorenz
    Institute of Pharmacology and Toxicology, University of Wurzburg, Versbacher Strasse 9, Wurzburg, Germany
    Nat Med 15:75-83. 2009
    ..We propose that specific phosphorylation events on ERK1/2 integrate differing upstream signals (Raf1-MEK1/2 or G protein-coupled receptor-G(q)) to induce cardiac hypertrophy...
  3. ncbi Cardiac hypertrophy: targeting Raf/MEK/ERK1/2-signaling
    Kristina Lorenz
    Institute of Pharmacology and Toxicology, University of Wurzburg, Versbacher Strasse 9, 97078 Wurzburg, Germany
    Int J Biochem Cell Biol 41:2351-5. 2009
    ..This short review will discuss new mechanistic insights into ERK1/2-dependent development of cardiac hypertrophy and the prospect to translate this knowledge into future therapeutic strategies...