'Location, location, location': activation and targeting of MAP kinases by G protein-coupled receptors.
A growing body of data supports the conclusion that G protein-coupled receptors can regulate cellular growth and differentiation by controlling the activity of MAP kinases. The activation of heterotrimeric G protein pools initiates a complex network of signals leading to MAP kinase activation that frequently involves cross-talk between G protein-coupled receptors and receptor tyrosine kinases or focal adhesions. The dominant mechanism of MAP kinase activation varies significantly between receptor and cell type. Moreover, the mechanism of MAP kinase activation has a substantial impact on MAP kinase function. Some signals lead to the targeting of activated MAP kinase to specific extranuclear locations, while others activate a MAP kinase pool that is free to translocate to the nucleus and contribute to a mitogenic response.
Luttrell
L M
LM
Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA. luttrell@receptor-biol.duke.edu
D000818:Animals; D019390:Arrestins / Q000378:metabolism; D004789:Enzyme Activation; D020962:Heterotrimeric GTP-Binding Proteins / Q000378:metabolism; D020935:MAP Kinase Signaling System / Q000502:physiology*; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D021122:Protein Subunits / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism*; D000071557:beta-Arrestins
D019390:Arrestins; D021122:Protein Subunits; D043562:Receptors, G-Protein-Coupled; D000071557:beta-Arrestins; D020928:Mitogen-Activated Protein Kinases; D020962:Heterotrimeric GTP-Binding Proteins