The role of G-protein coupled receptors and associated proteins in receptor tyrosine kinase signal transduction

Catherine Waters, Susan Pyne, Nigel J Pyne

Research output: Contribution to journalLiterature review

73 Citations (Scopus)

Abstract

It is well established that stimulation of G-protein coupled receptors (GPCRs) can activate signalling from receptor tyrosine kinases by a process termed transactivation. Indeed, in recent years, it has become apparent that transactivation is a general phenomenon that has been demonstrated for many unrelated GPCRs and receptor tyrosine kinases. In this case the GPCR/G-protein participation is up-stream of the receptor tyrosine kinase. Substantial research has addressed these findings but meanwhile another mechanism of cross talk has been slowly emerging. For over a decade, a growing body of evidence has demonstrated that numerous growth factors use G-proteins and attendant signalling molecules such as beta-arrestins that participate down-stream of the receptor tyrosine kinase to signal to effectors, such as p42/p44 MAPK. This review highlights this novel mechanism of cross talk between receptor tyrosine kinases and GPCRs, which is distinct from growth factor receptor transactivation by GPCRs.
Original languageEnglish
Pages (from-to)309-323
Number of pages15
JournalSeminars in Cell and Developmental Biology
Volume15
Issue number3
DOIs
Publication statusPublished - Jun 2004

Fingerprint

Receptor Protein-Tyrosine Kinases
G-Protein-Coupled Receptors
Signal Transduction
Transcriptional Activation
GTP-Binding Proteins
Receptor Cross-Talk
Mitogen-Activated Protein Kinase 3
Growth Factor Receptors
Mitogen-Activated Protein Kinase 1
Intercellular Signaling Peptides and Proteins
Research

Keywords

  • humans
  • phosphorylation
  • receptor protein-tyrosine Kinases
  • receptors, G-protein-coupled
  • signal transduction
  • transcriptional activation

Cite this

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The role of G-protein coupled receptors and associated proteins in receptor tyrosine kinase signal transduction. / Waters, Catherine; Pyne, Susan; Pyne, Nigel J.

In: Seminars in Cell and Developmental Biology , Vol. 15, No. 3, 06.2004, p. 309-323.

Research output: Contribution to journalLiterature review

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AU - Waters, Catherine

AU - Pyne, Susan

AU - Pyne, Nigel J

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AB - It is well established that stimulation of G-protein coupled receptors (GPCRs) can activate signalling from receptor tyrosine kinases by a process termed transactivation. Indeed, in recent years, it has become apparent that transactivation is a general phenomenon that has been demonstrated for many unrelated GPCRs and receptor tyrosine kinases. In this case the GPCR/G-protein participation is up-stream of the receptor tyrosine kinase. Substantial research has addressed these findings but meanwhile another mechanism of cross talk has been slowly emerging. For over a decade, a growing body of evidence has demonstrated that numerous growth factors use G-proteins and attendant signalling molecules such as beta-arrestins that participate down-stream of the receptor tyrosine kinase to signal to effectors, such as p42/p44 MAPK. This review highlights this novel mechanism of cross talk between receptor tyrosine kinases and GPCRs, which is distinct from growth factor receptor transactivation by GPCRs.

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KW - signal transduction

KW - transcriptional activation

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