A new G(q)-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.
Gutkind
J Silvio
JS
Offermanns
Stefan
S
D000818:Animals; D001665:Binding Sites; D002467:Cell Nucleus / Q000378:metabolism; D043802:GTP-Binding Protein alpha Subunits, Gq-G11 / Q000378:metabolism*; D005786:Gene Expression Regulation; D006321:Heart / Q000502:physiology*; D006801:Humans; D020935:MAP Kinase Signaling System; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D008954:Models, Biological; D009206:Myocardium / Q000378:metabolism*; D019899:Paracrine Communication; D010766:Phosphorylation; D015398:Signal Transduction
D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D043802:GTP-Binding Protein alpha Subunits, Gq-G11