共 31 条
PKD is recruited to sites of actin remodelling at the leading edge and negatively regulates cell migration
被引:52
作者:

Eiseler, Tim
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Univ Stuttgart, Inst Cell Biol & Immunol, D-70569 Stuttgart, Germany Univ Stuttgart, Inst Cell Biol & Immunol, D-70569 Stuttgart, Germany

Schmid, Michael A.
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Univ Stuttgart, Inst Cell Biol & Immunol, D-70569 Stuttgart, Germany Univ Stuttgart, Inst Cell Biol & Immunol, D-70569 Stuttgart, Germany

Topbas, Fitnat
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Univ Stuttgart, Inst Cell Biol & Immunol, D-70569 Stuttgart, Germany Univ Stuttgart, Inst Cell Biol & Immunol, D-70569 Stuttgart, Germany

Pfizenmaier, Klaus
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Univ Stuttgart, Inst Cell Biol & Immunol, D-70569 Stuttgart, Germany Univ Stuttgart, Inst Cell Biol & Immunol, D-70569 Stuttgart, Germany

Hausser, Angelika
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Univ Stuttgart, Inst Cell Biol & Immunol, D-70569 Stuttgart, Germany Univ Stuttgart, Inst Cell Biol & Immunol, D-70569 Stuttgart, Germany
机构:
[1] Univ Stuttgart, Inst Cell Biol & Immunol, D-70569 Stuttgart, Germany
关键词:
actin remodelling;
cell migration;
F-actin interaction;
phosphorylation leading edge;
D O I:
10.1016/j.febslet.2007.07.079
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
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. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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页码:4279 / 4287
页数:9
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