Joachim P Schmitt
- Alterations of phospholamban function can exhibit cardiotoxic effects independent of excessive sarcoplasmic reticulum Ca2+-ATPase inhibitionJoachim 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...
- A new type of ERK1/2 autophosphorylation causes cardiac hypertrophyKristina 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...
- Cardiac hypertrophy: targeting Raf/MEK/ERK1/2-signalingKristina 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...
- β-Myosin Heavy Chain Variant Val606Met Causes Very Mild Hypertrophic Cardiomyopathy in Mice, but Exacerbates HCM Phenotypes in Mice Carrying Other HCM MutationsRobert Blankenburg
From the Institute of Pharmacology and Toxicology, University of Wurzburg, Wurzburg, Germany R B, S W, M J L, J P S Institute of Pharmacology and Clinical Pharmacology, University Hospital Düsseldorf and Cardiovascular Research Institute Düsseldorf CARID, Heinrich Heine University, Dusseldorf, Germany K H, J P S Cardiovascular Division, Brigham and Women s Hospital, Boston, MA C E S Department of Genetics, Harvard Medical School, Boston, MA J G S and Bio Medical Research Center BMFZ, Heinrich Heine University, Dusseldorf, Germany R D
Circ Res 115:227-37. 2014..Associating disease phenotype with mutation is confounded by extensive background genetic and lifestyle/environmental differences between subjects even from the same family...