GPCR-jacking: from a new route in RTK signalling to a new concept in GPCR activation

Nicolas Delcourt1, Joël Bockaert, Philippe Marin

  • 1Institut de Génomique Fonctionnelle, Universités de Montpellier, CNRS UMR 5203, 141 rue de la Cardonille, Montpellier CEDEX 5, F-34094, France.

Insights

G protein-coupled receptors (GPCRs) and receptor tyrosine kinases (RTKs) signaling pathways extensively cross-talk. This review details the molecular mechanisms of GPCR-RTK transactivation and its role in cell growth.

Area of Science:

  • Cellular Biology
  • Molecular Signaling
  • Biochemistry

Background:

  • G protein-coupled receptors (GPCRs) and receptor tyrosine kinases (RTKs) are key cell surface receptors.
  • GPCR agonists can activate RTKs independently of growth factors, a process termed transactivation.
  • Emerging evidence shows RTKs can also activate GPCRs, indicating bidirectional signaling.

Purpose of the Study:

  • To provide an overview of the molecular mechanisms underlying GPCR-RTK cross-communication.
  • To discuss the relevance of this cross-talk in growth factor signaling and cellular functions.

Main Methods:

  • Literature review of existing studies on GPCR-RTK interactions.
  • Analysis of molecular pathways involved in transactivation.
  • Discussion of integrated signaling networks.

Main Results:

  • GPCRs can transactivate RTKs, contributing to growth-promoting activities.
  • RTKs can activate GPCRs, either ligand-dependently or independently.
  • This cross-communication forms an integrated signaling network.

Conclusions:

  • The bidirectional cross-talk between GPCRs and RTKs is a significant biological phenomenon.
  • Understanding these molecular mechanisms is crucial for elucidating growth factor signaling pathways and functions.

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