A New Gq-Initiated MAPK Signaling Pathway in the Heart
Copyright policy )A New Gq-Initiated MAPK Signaling Pathway in the Heart
Pathological cardiac hypertrophy involves auto/paracrine mediators acting through G(q/11)-coupled receptors. A novel signaling route stimulated by betagamma-subunits of G(q/11) results in the autophosphorylation of ERK1/2 on a new site and the nuclear retention of ERK1/2, thereby activating hypertrophic gene programs.
- National Institute of Health Pakistan
- Max Planck Society Germany
- Max Planck Institute for Heart and Lung Research Germany
- National Institutes of Health United States
- Heidelberg University Germany
Cell Nucleus, Mitogen-Activated Protein Kinase 1, Binding Sites, Mitogen-Activated Protein Kinase 3, MAP Kinase Signaling System, Myocardium, Heart, Models, Biological, Gene Expression Regulation, Paracrine Communication, Animals, GTP-Binding Protein alpha Subunits, Gq-G11, Humans, Phosphorylation, Developmental Biology, Signal Transduction
Cell Nucleus, Mitogen-Activated Protein Kinase 1, Binding Sites, Mitogen-Activated Protein Kinase 3, MAP Kinase Signaling System, Myocardium, Heart, Models, Biological, Gene Expression Regulation, Paracrine Communication, Animals, GTP-Binding Protein alpha Subunits, Gq-G11, Humans, Phosphorylation, Developmental Biology, Signal Transduction
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