Raf-1: a novel cardiac troponin T kinase
| Autor: | Susan F. Steinberg, Chaojian Wang, Vitalyi O. Rybin, Paul Pfleiderer, Marius P. Sumandea |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Threonine
inorganic chemicals Indoles Physiology macromolecular substances Mitogen-activated protein kinase kinase Biochemistry Article Phenols Troponin T Troponin complex Troponin I Animals Myocytes Cardiac Phosphorylation Rats Wistar Kinase activity Rho-associated protein kinase Cells Cultured Protein kinase C Chemistry Cell Biology Myocardial Contraction Molecular biology Recombinant Proteins Rats Proto-Oncogene Proteins c-raf enzymes and coenzymes (carbohydrates) cardiovascular system bacteria PRKCE |
| Zdroj: | Journal of Muscle Research and Cell Motility. 30:67-72 |
| ISSN: | 1573-2657 0142-4319 |
| DOI: | 10.1007/s10974-009-9176-y |
| Popis: | Phosphorylation of cardiac troponin is a key mechanism involved in regulation of contractile function. In vitro kinase assays revealed that lysates prepared from resting cardiomyocytes contain cardiac troponin I (cTnI) and cTnT kinase activity. cTnI phosphorylation is inhibited by pharmacologic inhibitors of PKA, PKC, Rho kinase and PKC effectors such as RSK and PKD; these kinase inhibitors do not inhibit phosphorylation of cTnT. Rather, cTnT phosphorylation is decreased by the Raf inhibitor GW5074. In vitro kinase assays show that recombinant Raf phosphorylates cTnT, and that Raf-dependent cTnT phosphorylation is abrogated by a T206E substitution; Raf does not phosphorylate cTnI. These studies identify Raf-dependent cTnT-Thr(206) phosphorylation as a novel mechanism that would link growth factor-dependent signaling pathways to dynamic changes in cardiac contractile function. |
| Databáze: | OpenAIRE |
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