Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 281, Issue 15, Pages 10583-10588Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M513002200
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- NIA NIH HHS [AG 014563] Funding Source: Medline
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Tyrosine kinase Csk is essential for mouse embryonic development. Csk knock-out mice died at early stages of embryogenesis ( around embryonic day 10). The molecular mechanism for this defect is not completely understood. Here we report that Csk deficiency in mouse embryonic fibroblast cells blocked cell migration induced by lysophosphatidic acid through G protein-coupled receptors, by platelet-derived growth factor and epidermal growth factor through receptor tyrosine kinases, and by serum. Re-expression of Csk in these Csk-deficient cells rescued the migratory phenotype. Furthermore, deletion of Csk did not interfere with Rac activation and lamellipodia formation, but impaired the focal adhesions. Our data demonstrate a critical role for Csk in cell migration.
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