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首页> 外文期刊>Journal of cellular physiology. >Differential phosphorylation regulates the shear stress-induced polar activity of Rho-specific guanine nucleotide dissociation inhibitor α
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Differential phosphorylation regulates the shear stress-induced polar activity of Rho-specific guanine nucleotide dissociation inhibitor α

机译：微分磷酸化调节剪切压力诱导极性Rho-specific活动鸟嘌呤核苷酸分解抑制剂α

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The activity of Rho-specific guanine nucleotide dissociation inhibitor α (RhoGD1α) is regulated by its own phosphorylation at different amino acid sites. These phosphorylation sites may have a crucial role in local Rho GTPases activation during cell migration. This paper is designed to explore the influence of phosphorylation on shear stress-induced spatial RhoGDIa activation. Based on the fluorescence resonance energy transfer biosensor sl-RhoGDIα, which was constructed to test the RhoGDIa activity in living cells, new RhoGDIa phosphomimetic mutation (sl-S101E/S174E, sl-Y156E, sl-S101E, sl-S174E) and phosphorylation-deficient mutation (sl-S101A/S174A, sl-Y156A, sl-S101A, sl-S174A) biosensors were designed to test their effects on RhoGDIa activation upon shear stress application in human umbilical vein endothelial cells (HUVECs). The results showed lower RhoGDIa activity at the downstream of HUVECs (the region from the edge of the nucleus to the edge of the cell along with the flow). The overall decrease in RhoGDIa activity was inhibited by Y156A-mutant, whereas the polarized RhoGDIa and Racl activity were blocked by S101A/S174A mutant. It is concluded that the Tyrl56 phosphorylation mainly mediates shear stress-induced overall RhoGDIa activity, while Ser101/Serl74 phosphorylation mediates its polarization. This study demonstrates that differential phosphorylation of RhoGDIa regulates shear stress-induced spatial RhoGDIa activation, which could be a potential target to control cell migration.
机译：Rho-specific鸟嘌呤核苷酸的活动分离抑制剂α(RhoGD1α)监管在不同的氨基酸的磷酸化酸的网站。在当地ρgtpase激活了至关重要的作用在细胞迁移。探索在剪切磷酸化的影响空间RhoGDIa应激激活。荧光共振能量转移生物传感器sl-RhoGDIα,构造在活细胞中测试RhoGDIa活动、新RhoGDIa phosphomimetic突变(sl-S101E / S174E,sl-Y156E sl-S101E sl-S174E)和phosphorylation-deficient突变(sl-S101A / S174A sl-Y156A、sl-S101A sl-S174A)生物传感器是为了测试他们的影响RhoGDIa激活在剪切应力的应用程序在人类脐静脉内皮细胞(HUVECs)。活动的下游HUVECs(该地区从核的边缘的边缘细胞随流)。在RhoGDIa活动受到抑制Y156A-mutant,而极化RhoGDIa和射氯活动被S101A / S174A突变。结果表明,Tyrl56磷酸化主要介导剪切压力引起的整体RhoGDIa活动,同时Ser101 / Serl74磷酸化调节其极化。研究表明,微分RhoGDIa的磷酸化调节剪切空间RhoGDIa应激激活,可能是一个潜在的目标控制细胞迁移。

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