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Vol. 10, Issue 3, 551-565, March 1999
*Centre National de la Recherche Scientifique EP 560, Institut de Biologie de Lille, Institut Pasteur de Lille, 59021 Lille,
France; and The scatter factor/hepatocyte growth factor regulates scattering
and morphogenesis of epithelial cells through activation of the MET
tyrosine kinase receptor. In particular, the noncatalytic C-terminal
tail of MET contains two autophosphorylation tyrosine residues, which
form a multisubstrate-binding site for several cytoplasmic effectors
and are thought to be essential for signal transduction. We show here
that a MET receptor mutated on the four C-terminal tyrosine residues,
Y1311F, Y1347F, Y1354F, and Y1363F, can induce efficiently a
transcriptional response and cell scattering, whereas it cannot induce
cell morphogenesis. Although the mutated receptor had lost its ability
to recruit and/or activate known signaling molecules, such as GRB2,
SHC, GAB1, and PI3K, by using a sensitive association-kinase assay we
found that the mutated receptor can still associate and phosphorylate a
~250-kDa protein. By further examining signal transduction mediated by the mutated MET receptor, we established that it can transmit efficient RAS signaling and that cell scattering by the mutated MET
receptor could be inhibited by a pharmacological inhibitor of the
MEK-ERK (MAP kinase kinase-extracellular signal-regulated kinase)
pathway. We propose that signal transduction by autophosphorylation of
the C-terminal tyrosine residues is not the sole mechanism by which the
activated MET receptor can transmit RAS signaling and cell scattering.
Department of Therapeutics/Biotechnology,
Boehringer Mannheim, 82372 Penzberg, Germany
Corresponding author. E-mail address:
vfafeur{at}infobiogen.fr.
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