多囊蛋白（PKD）被募集到前沿肌动蛋白重塑位点，并对细胞迁移起负向调节作用。
PKD is recruited to sites of actin remodelling at the leading edge and negatively regulates cell migration.
作者信息
Eiseler Tim, Schmid Michael A, Topbas Fitnat, Pfizenmaier Klaus, Hausser Angelika
机构信息
Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany.
出版信息
FEBS Lett. 2007 Sep 4;581(22):4279-87. doi: 10.1016/j.febslet.2007.07.079. Epub 2007 Aug 10.
Protein kinase D (PKD) has been implicated in the regulation of cell shape, adhesion, and migration. At the leading edge of migrating cells active PKD co-localizes with F-actin, Arp3 and cortactin. Platelet derived growth factor (PDGF) activates PKD and recruits the kinase to the leading edge, suggesting a role for PKD in actin remodelling. In support of this, PKD directly interacts with F-actin and phosphorylates cortactin in vitro. Interference with PKD function by overexpression of a dominant negative PKD or by PKD-specific siRNA enhanced cell migration, whereas cells overexpressing PKD wild type displayed reduced migratory potential. Taken together, these data reveal a negative regulatory function of PKD in cell migration.
蛋白激酶D（PKD）参与细胞形状、黏附和迁移的调控。在迁移细胞的前沿，活性PKD与F-肌动蛋白、Arp3和皮层肌动蛋白共定位。血小板衍生生长因子（PDGF）激活PKD并将该激酶招募至前沿，提示PKD在肌动蛋白重塑中发挥作用。与此相符的是，PKD在体外直接与F-肌动蛋白相互作用并使皮层肌动蛋白磷酸化。通过过表达显性负性PKD或PKD特异性小干扰RNA（siRNA）干扰PKD功能可增强细胞迁移，而过度表达PKD野生型的细胞迁移潜能降低。综上所述，这些数据揭示了PKD在细胞迁移中的负调控功能。
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