Receptor tyrosine kinases are signaling intermediates of G protein-coupled receptors.
G protein-coupled receptors (GPCRs) can utilize receptor tyrosine kinases (RTKs) to mediate important cellular responses such as proliferation, differentiation and survival. Recent advances in the field suggest that GPCR-induced transactivation of RTKs might be important for diseases such as cancer and cardiac hypertrophy. Depending on the receptor and cell type, GPCR signaling involves activation of several different RTKs. By activating different subsets of RTKs, GPCRs can fine-tune their effects on target cells. Furthermore, RTK-independent signaling pathways also initiated by GPCRs may modify the biological read out of the transactivated RTKs. This review focuses on the mechanisms how GPCRs and intracellular messengers elicit transactivation of different RTKs and the resulting different biological responses.
Piiper
A
A
Department of Internal Medicine II, University of Saarland, D-66421 Homburg/Saar, Germany. inapii@uniklinik-saarland.de
Zeuzem
S
S
D002450:Cell Communication; D006801:Humans; D008024:Ligands; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism / Q000502:physiology*; D043562:Receptors, G-Protein-Coupled / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*; D015533:Transcriptional Activation
D008024:Ligands; D043562:Receptors, G-Protein-Coupled; D020794:Receptor Protein-Tyrosine Kinases