Role of tyrosine kinase Csk in G protein-coupled receptor- and receptor tyrosine kinase-induced fibroblast cell migration

Deirdre McGarrigle, Dandan Shan, Shengyu Yang, Xin Yun Huang

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)10583-10588
Number of pages6
JournalJournal of Biological Chemistry
Volume281
Issue number15
DOIs
StatePublished - Apr 14 2006

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Platelet-Derived Growth Factor
Receptor Protein-Tyrosine Kinases
Fibroblasts
G-Protein-Coupled Receptors
Epidermal Growth Factor
Protein-Tyrosine Kinases
Embryonic Development
Cell Movement
Adhesion
Chemical activation
Cells
Defects
Pseudopodia
Focal Adhesions
Epidermal Growth Factor Receptor
Knockout Mice
Phenotype
Serum
lysophosphatidic acid

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

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abstract = "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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Role of tyrosine kinase Csk in G protein-coupled receptor- and receptor tyrosine kinase-induced fibroblast cell migration. / McGarrigle, Deirdre; Shan, Dandan; Yang, Shengyu; Huang, Xin Yun.

In: Journal of Biological Chemistry, Vol. 281, No. 15, 14.04.2006, p. 10583-10588.

Research output: Contribution to journalArticle

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AU - McGarrigle, Deirdre

AU - Shan, Dandan

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