Integration of Signals from Receptor Tyrosine Kinases and G Protein-Coupled ReceptorsLowes V.L. · Ip N.Y. · Wong Y.H.
Department of Biochemistry, Biotechnology Research Institute and Molecular Neuroscience Center, Hong Kong University of Science and Technology, Hong Kong, China
Activation of G protein-coupled receptors (GPCRs) leads to stimulation of classical G protein signaling pathways. In addition, GPCRs can activate the mitogen-activated protein kinases (MAPKs) such as the extracellular signal-regulated kinases, c-Jun NH2-terminal kinases (JNKs), and p38 MAPKs, and thereby influence cell proliferation, cell differentiation and mitogenesis. Cross talk between GPCRs and receptor tyrosine kinases (RTKs) is an incredibly complex process, and the exact signaling molecules involved are largely dependent on the cell type and the type of receptor that is activated. In this review we investigate recent advances that have been made in understanding the mechanisms of cross talk between GPCRs and RTKs, with a focus on GPCR-mediated activation of the Ras/MAPK pathway, GPCR-induced transactivation of RTKs, GPCR-mediated activation of JNK, and p38 MAPK, integration of signals by RhoGTPases, and activation of G protein signaling pathways by RTKs.
© 2002 S. Karger AG, Basel
Yung H. Wong
Department of Biochemistry and Biotechnology Research Institute
Hong Kong University of Science and Technology
Clear Water Bay, Kowloon, Hong Kong (China)
Tel. +852 2358 7328, Fax +852 2358 1552, E-Mail firstname.lastname@example.org
Number of Print Pages : 15
Number of Figures : 2, Number of Tables : 0, Number of References : 114
Founded 1992 as ‘Biological Signals’ by S.F. Pang (1992–2001) continued as ‘Biological Signals and Receptors’ (1999–2001)
Vol. 11, No. 1, Year 2002 (Cover Date: January-February 2002)
Journal Editor: Nancy Y. Ip, Hong Kong
ISSN: 1424–862X (print), 1424–8638 (Online)
For additional information: http://www.karger.com/journals/nsg