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Imaging G-protein Coupled Receptor (GPCR)-mediated Signaling Events that Control Chemotaxis of Dictyostelium Discoideum
09:40

Imaging G-protein Coupled Receptor (GPCR)-mediated Signaling Events that Control Chemotaxis of Dictyostelium Discoideum

Published on: September 20, 2011

FES kinase participates in KIT-ligand induced chemotaxis

Edwige Voisset1, Sophie Lopez, Amandine Chaix

  • 1INSERM U891, Centre de Recherche en Cancérologie de Marseille (CRCM), Marseille, France. Edwige.Voisset@inserm.fr

Biochemical and Biophysical Research Communications
|February 2, 2010
PubMed

Insights

FES kinase mediates wild-type KIT signaling for cell migration, unlike its role in oncogenic KIT mutants. This study clarifies FES

Area of Science:

  • Cellular Biology
  • Molecular Oncology
  • Signal Transduction

Background:

  • FES (Friend of FES) is a cytoplasmic tyrosine kinase known as a viral oncogene product.
  • FES has been identified as a key effector in oncogenic KIT mutant receptor signaling.
  • The role of FES in wild-type KIT receptor function remains largely uncharacterized.

Purpose of the Study:

  • To investigate the interaction and functional role of FES in wild-type KIT receptor signaling.
  • To determine if FES is involved in proliferation and cell adhesion downstream of wild-type KIT.
  • To elucidate the specific contribution of FES to KIT-mediated cellular processes.

Main Methods:

  • Co-immunoprecipitation assays to assess FES-KIT interaction.
  • Western blotting to detect FES phosphorylation upon SCF stimulation.
  • Cell migration assays (chemotaxis) to evaluate the functional role of FES in wild-type KIT signaling.

Main Results:

  • FES interacts with and is phosphorylated by the wild-type KIT receptor upon stem cell factor (SCF) ligand binding.
  • FES is not implicated in wild-type KIT-mediated cell proliferation or adhesion.
  • FES is essential for SCF-induced chemotaxis, indicating its role in cell migration.

Conclusions:

  • FES kinase acts as a mediator of wild-type KIT signaling pathways.
  • FES specifically regulates KIT-dependent cell migration, distinct from its role in oncogenic KIT signaling.
  • These findings highlight a novel function of FES in normal cellular processes regulated by KIT.

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