Protein tyrosine kinase-mediated pathways in G protein-coupled receptor signaling.
Abundant evidence has indicated that protein tyrosine kinases (PTKs) convey signals from G protein-coupled receptors (GPCRs) to regulate cell proliferation, migration, adhesion, and potentially cellular transformation. Molecular mechanisms by which PTKs regulate such diverse effects in GPCR signaling are not well understood. Recently, an unifying theme has emerged where both growth factors and GPCRs utilize protein tyrosine kinase activity and the highly conserved Ras/MAP kinase pathway to control mitogenic signals. Additionally, PTKs are also involved in the regulation of signal transmission from GPCRs to activation of the JNK/SAPK kinase pathway. Furthermore novel insights in chemokine receptor-activated PTKs and their role in mediating cell functions are discussed in this review.
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Ludwig Institute for Cancer Research, Uppsala, Sweden.
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D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000378:metabolism / Q000502:physiology; D002455:Cell Division; D004789:Enzyme Activation; D019204:GTP-Binding Proteins / Q000502:physiology*; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases; D020928:Mitogen-Activated Protein Kinases; D008954:Models, Biological; D011505:Protein-Tyrosine Kinases / Q000378:metabolism*; D011956:Receptors, Cell Surface / Q000502:physiology*; D019707:Receptors, Chemokine / Q000502:physiology; D012441:Saccharomyces cerevisiae / Q000201:enzymology; D015398:Signal Transduction; D014407:Tumor Cells, Cultured
D011956:Receptors, Cell Surface; D019707:Receptors, Chemokine; D011505:Protein-Tyrosine Kinases; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D048031:JNK Mitogen-Activated Protein Kinases; D020928:Mitogen-Activated Protein Kinases; D019204:GTP-Binding Proteins