Reduced cell motility and enhanced focal adhesion contact formation in cells from FAK-deficient mice
Reduced cell motility and enhanced focal adhesion contact formation in cells from FAK-deficient mice
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DOI：
10.1038/377539a0
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发表时间：
1995-01-01
期刊：
影响因子：
--
通讯作者：
Aizawa, Shinichi
中科院分区：
文献类型：
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作者：
Ilic, Dusko;Furuta, Tasuhide;Aizawa, Shinichi
细胞内蛋白酪氨酸激酶 FAK（粘着斑激酶）最初是通过其在 v-src 转化细胞中的高水平酪氨酸磷酸化而被识别的。 FAK 在早期发育过程中也高度磷酸化。在培养的细胞中，它定位于粘着斑接触处，并响应整合素介导的细胞与细胞外基质的结合而被磷酸化和激活，这表明在细胞粘附和/或迁移中发挥重要作用。我们通过基因打靶培育出 FAK 缺陷小鼠，以检查 FAK 在发育过程中的作用。突变胚胎表现出中胚层发育的普遍缺陷，并且来自这些胚胎的细胞在体外的流动性降低。令人惊讶的是，FAK 缺陷细胞中粘着斑的数量增加，表明 FAK 可能参与细胞迁移过程中粘着斑接触的周转。
The intracellular protein tyrosine kinase FAK (focal adhesion kinase) was originally identified by its high level of tyrosine phosphorylation in v-src-transformed cells. FAK is also highly phosphorylated during early development. In cultured cells it is localized to focal adhesion contacts and becomes phosphorylated and activated in response to integrin-mediated binding of cells to the extracellular matrix, suggesting an important role in cell adhesion and/or migration. We have generated FAK-deficient mice by gene targeting to examine the role of FAK during development. Mutant embryos displayed a general defect of mesoderm development, and cells from these embryos had reduced mobility in vitro. Surprisingly, the number of focal adhesions was increased in FAK-deficient cells, suggesting that FAK may be involved in the turnover of focal adhesion contacts during cell migration.