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J Biol Chem, Vol. 274, Issue 36, 25726-25734, September 3, 1999
From the Department of Medical Biochemistry and Microbiology,
Uppsala University Biomedical Center, Box 575, S-751 23 Uppsala, Sweden
Stimulation of fibroblast growth factor
receptor-1 (FGFR-1) expressed on endothelial cells leads to cellular
migration and proliferation. We have examined the role of the Src
homology (SH) 2/SH3 domain-containing adaptor protein Crk in these
processes. Transient tyrosine phosphorylation of Crk in fibroblast
growth factor-2-stimulated endothelial cells was dependent on the
juxtamembrane tyrosine residue 463 in FGFR-1, and a Crk SH2 domain
precipitated FGFR-1 via phosphorylated Tyr-463, indicating direct
complex formation between Crk and FGFR-1. Furthermore, Crk SH2 and SH3
domains formed ligand-independent complexes with Shc, C3G, and the
Crk-associated substrate (Cas). Tyrosine phosphorylation of C3G and Cas
increased as a consequence of growth factor treatment. We examined the
role of Crk in FGFR-1-mediated cellular responses by use of cells
expressing chimeric platelet-derived growth factor receptor-
Fibroblast Growth Factor Receptor-1-mediated Endothelial Cell
Proliferation Is Dependent on the Src Homology (SH) 2/SH3
Domain-containing Adaptor Protein Crk
/FGFR-1
(R/FR) wild type and mutant Y463F receptors. The kinase activity of
R/FR Y463F was intact, but both Crk and the adaptor FRS-2 were no
longer tyrosine-phosphorylated in the mutant cells. Both wild type and mutant receptor cells migrated efficiently, whereas cells expressing the mutant R/FR Y463F failed to proliferate and Erk2 and Jun kinase
activities were suppressed in these cells. In wild type R/FR cells
transiently expressing an SH2 domain mutant of Crk, Erk and Jun kinase
activities as well as DNA synthesis were attenuated. Our data indicate
that Crk participates in signaling complexes downstream of FGFR-1,
which propagate mitogenic signals.
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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