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首页> 外文期刊>Molecular and Cellular Biology >c-Src-Mediated Phosphorylation of TRIP6 Regulates Its Function in Lysophosphatidic Acid-Induced Cell Migration
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c-Src-Mediated Phosphorylation of TRIP6 Regulates Its Function in Lysophosphatidic Acid-Induced Cell Migration

机译：c-Src介导的TRIP6磷酸化调节其在溶血磷脂酸诱导的细胞迁移中的功能。

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TRIP6 (thyroid receptor-interacting protein 6), also known as ZRP-1 (zyxin-related protein 1), is a member of the zyxin family that has been implicated in cell motility. Previously we have shown that TRIP6 binds to the LPA2 receptor and associates with several components of focal complexes in an agonist-dependent manner and, thus, enhances lysophosphatidic acid (LPA)-induced cell migration. Here we further report that the function of TRIP6 in LPA signaling is regulated by c-Src-mediated phosphorylation of TRIP6 at the Tyr-55 residue. LPA stimulation induces tyrosine phosphorylation of endogenous TRIP6 in NIH 3T3 cells and c-Src-expressing fibroblasts, which is virtually eliminated in Src-null fibroblasts. Strikingly, both phosphotyrosine-55 and proline-58 residues of TRIP6 are required for Crk binding in vitro and in cells. Mutation of Tyr-55 to Phe does not alter the ability of TRIP6 to localize at focal adhesions or associate with actin. However, it abolishes the association of TRIP6 with Crk and p130cas in cells and significantly reduces the function of TRIP6 to promote LPA-induced ERK activation. Ultimately, these signaling events control TRIP6 function in promoting LPA-induced morphological changes and cell migration.
机译：TRIP6（与 p rotein 6相互作用的 t hyroid r 受体 i ），也称为ZRP-1（zyxin） -相关蛋白1），是与细胞运动有关的zyxin家族成员。先前我们已经证明，TRIP6结合LPA 2 受体，并以激动剂依赖性方式与局灶复合物的几个组分缔合，从而增强了溶血磷脂酸（LPA）诱导的细胞迁移。在这里，我们进一步报告，TRIP6在LPA信号中的功能受c-Src介导的Tyr-55残基上TRIP6的磷酸化作用的调节。 LPA刺激在NIH 3T3细胞和表达c-Src的成纤维细胞中诱导内源性TRIP6的酪氨酸磷酸化，而实际上在Src-null的成纤维细胞中已被消除。引人注目的是，TRIP6的磷酸酪氨酸55和脯氨酸58残基在体外和细胞中都需要Crk结合。 Tyr-55突变为Phe不会改变TRIP6定位于粘着斑或与肌动蛋白结合的能力。但是，它消除了TRIP6与细胞中Crk和p130 cas 的关联，并显着降低了TRIP6促进LPA诱导的ERK活化的功能。最终，这些信号事件控制了TRIP6在促进LPA诱导的形态变化和细胞迁移中的功能。

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