Role of tyrosine kinase Csk in G protein-coupled receptor- and receptor tyrosine kinase-induced fibroblast cell migration
Role of tyrosine kinase Csk in G protein-coupled receptor- and receptor tyrosine kinase-induced fibroblast cell migration
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DOI：
10.1074/jbc.m513002200
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发表时间：
2006-04-14
影响因子：
4.8
通讯作者：
Huang, XY
中科院分区：
文献类型：
--
作者：
McGarrigle, D;Shan, DD;Huang, XY
酪氨酸激酶Csk对小鼠胚胎发育至关重要。Csk基因敲除小鼠在胚胎发育的早期阶段（大约胚胎第10天）死亡。这种缺陷的分子机制尚未完全了解。在这里，我们报告，小鼠胚胎成纤维细胞中的Csk缺乏症阻断细胞迁移诱导溶血磷脂酸通过G蛋白偶联受体，血小板衍生生长因子和表皮生长因子通过受体酪氨酸激酶，和血清。在这些Csk缺陷细胞中重新表达Csk拯救了迁移表型。此外，Csk的缺失并不干扰Rac的激活和板状伪足的形成，但会损害局灶性粘连。我们的数据表明Csk在细胞迁移中起关键作用。
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.