FES kinase participates in KIT-ligand induced chemotaxis.
FES is a cytoplasmic tyrosine kinase activated by several membrane receptors, originally identified as a viral oncogene product. We have recently identified FES as a crucial effector of oncogenic KIT mutant receptor. However, FES implication in wild-type KIT receptor function was not addressed. We report here that FES interacts with KIT and is phosphorylated following activation by its ligand SCF. Unlike in the context of oncogenic KIT mutant, FES is not involved in wild-type KIT proliferation signal, or in cell adhesion. Instead, FES is required for SCF-induced chemotaxis. In conclusion, FES kinase is a mediator of wild-type KIT signalling implicated in cell migration.
Voisset
Edwige
E
INSERM U891, Centre de Recherche en Cancérologie de Marseille (CRCM), Marseille, France. Edwige.Voisset@inserm.fr
Lopez
Sophie
S
Chaix
Amandine
A
Vita
Marina
M
George
Coralie
C
Dubreuil
Patrice
P
De Sepulveda
Paulo
P
D002448:Cell Adhesion; D045744:Cell Line, Tumor; D002633:Chemotaxis; D006801:Humans; D010766:Phosphorylation; D051578:Proto-Oncogene Proteins c-fes / Q000235:genetics / Q000378:metabolism*; D019089:Stem Cell Factor / Q000378:metabolism*; D020798:Two-Hybrid System Techniques; D014443:Tyrosine; D018909:src Homology Domains
D019089:Stem Cell Factor; D014443:Tyrosine; D051578:Proto-Oncogene Proteins c-fes