@article{3090285,
    title = "Differential roles of MAPKs and MSK1 signalling pathways in the regulation of c-Jun during phenylephrine-induced cardiac myocyte hypertrophy",
    author = "Markou, T. and Cieslak, D. and Gaitanaki, C. and Lazou, A.",
    journal = "Molecular and Cellular Biochemistry",
    year = "2009",
    volume = "322",
    number = "1-2",
    pages = "103-112",
    issn = "0300-8177",
    doi = "10.1007/s11010-008-9945-8",
    keywords = "messenger RNA;  mitogen activated protein kinase;  mitogen activated protein kinase 3;  phenylephrine;  protein c jun;  stress activated protein kinase;  stress activated protein kinase 1;  synaptophysin, animal cell;  animal experiment;  animal model;  article;  cell activation;  cell stimulation;  controlled study;  gene activation;  gene control;  gene function;  gene interaction;  heart muscle cell;  heart ventricle hypertrophy;  male;  nonhuman;  nucleotide sequence;  pathogenesis;  protein phosphorylation;  rat;  signal transduction;  upregulation, Animals;  Cardiomegaly;  Cell Enlargement;  JNK Mitogen-Activated Protein Kinases;  Male;  MAP Kinase Signaling System;  Mitogen-Activated Protein Kinase 1;  Mitogen-Activated Protein Kinase 3;  Mitogen-Activated Protein Kinases;  Myocytes, Cardiac;  Phenylephrine;  Phosphorylation;  Proto-Oncogene Proteins c-jun;  Rats;  Ribosomal Protein S6 Kinases, 90-kDa;  RNA, Messenger;  Up-Regulation",
    abstract = "Gq-protein-coupled receptor (GqPCR) signalling is associated with the induction of cardiac myocyte hypertrophy, which is characterized by an increase in expression of immediate early genes via activation of pre-existing transcription factors. Here, we explore the role of MSK1 and MAPK signalling pathways in the regulation of the immediate early gene c-jun. The results provide further support for the role of MSK1 in cardiac myocyte hypertrophy and indicate that PE activates distinct signalling mechanisms which culminate with a complex activation of c-jun. ERK1/2 and JNKs are the principal kinases responsible for phosphorylation of c-Jun, whereas c-jun mRNA and protein up-regulation by PE is mediated by multiple signalling pathways that include MSK1, ERK1/2, p38-MAPK and JNKs. These signalling mechanisms seem to be critical to the phenotypic changes of cardiac myocytes in response to hypertrophic stimulation. © Springer Science+Business Media, LLC. 2008."
}