Diacylglycerol kinase γ interacts with and activates β2‐chimaerin, a Rac‐specific GAP, in response to epidermal growth factor
Diacylglycerol kinase γ interacts with and activates β2‐chimaerin, a Rac‐specific GAP, in response to epidermal growth factor
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DOI：
10.1016/j.febslet.2007.01.022
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发表时间：
2007-02
期刊：
影响因子：
3.5
通讯作者：
S. Yasuda;M. Kai;S. Imai;H. Kanoh;F. Sakane
中科院分区：
文献类型：
--
作者：
S. Yasuda;M. Kai;S. Imai;H. Kanoh;F. Sakane
研究表明，二酰基甘油激酶(DGK)γ是Rac1的上游抑制剂。在本文中，我们报道了在表皮生长因子刺激的COS7细胞中，DGKγ与β2-嵌合体(GAP)特异性地相互作用并共同定位于质膜。此外，DGKγ可促进β-2嵌合体依赖于表皮生长因子的转位至质膜。有趣的是，DGKγ通过其催化作用显著增强β2-嵌合体的依赖于表皮生长因子的GAP活性。这些结果表明，Dgkγ是一种新的β2-嵌合体调节因子，提示β2-嵌合体是一种效应分子，在功能上将Dgkγ与Rac1连接。
Diacylglycerol kinase (DGK)γ was shown to act as an upstream suppressor of Rac1. Here we report that, in COS7 cells stimulated with epidermal growth factor (EGF), DGKγ specifically interacts and co-localizes at the plasma membrane with β2-chimaerin, a GTPase-activating protein (GAP) for Rac. Moreover, DGKγ enhanced EGF-dependent translocation of β2-chimaerin to the plasma membrane. Interestingly, DGKγ markedly augmented EGF-dependent GAP activity of β2-chimaerin through its catalytic action. These results indicate that DGKγ is a novel regulator of β2-chimaerin, and thus suggest that β2-chimaerin is an effector molecule, linking DGKγ functionally with Rac1.