Transactivation joins multiple tracks to the ERK/MAPK cascade.
Many agonists of G-protein-coupled receptors (GPCRs) can stimulate receptor tyrosine kinases and the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) pathway. A 'transactivation' mechanism, which links these events in one signalling chain, inspired many researchers, but inevitably raised new questions. A 'multi-track' model for GPCR signalling to the ERK/MAPK pathway might resolve some of the puzzles in the transactivation field.
Wetzker
Reinhard
R
Institute for Molecular Cell Biology, Jena University Hospital, Drackendorfer Strasse 1, D-07747 JENA, Germany. i5rewe@rz.uni-jena.de
Böhmer
Frank-D
FD
D000818:Animals; D004789:Enzyme Activation; D066246:ErbB Receptors / Q000378:metabolism; D019204:GTP-Binding Proteins / Q000378:metabolism*; D006801:Humans; D020935:MAP Kinase Signaling System / Q000502:physiology*; D008666:Metalloendopeptidases / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D008954:Models, Biological
D066246:ErbB Receptors; D020928:Mitogen-Activated Protein Kinases; D008666:Metalloendopeptidases; D019204:GTP-Binding Proteins