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蛋白激酶D通过在高尔基体复合体上磷酸化并激活磷脂酰肌醇-4激酶IIIβ来调节囊泡运输。

Protein kinase D regulates vesicular transport by phosphorylating and activating phosphatidylinositol-4 kinase IIIbeta at the Golgi complex.

作者信息

Hausser Angelika, Storz Peter, Märtens Susanne, Link Gisela, Toker Alex, Pfizenmaier Klaus

机构信息

Institute for Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany.

出版信息

Nat Cell Biol. 2005 Sep;7(9):880-6. doi: 10.1038/ncb1289. Epub 2005 Aug 14.

DOI:10.1038/ncb1289
PMID:16100512
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1458033/
Abstract

Protein kinase D (PKD) regulates the fission of vesicles originating from the trans-Golgi network. We show that phosphatidylinositol 4-kinase IIIbeta (PI4KIIIbeta) - a key player in the structure and function of the Golgi complex - is a physiological substrate of PKD. Of the three PKD isoforms, only PKD1 and PKD2 phosphorylated PI4KIIIbeta at a motif that is highly conserved from yeast to humans. PKD-mediated phosphorylation stimulated lipid kinase activity of PI4KIIIbeta and enhanced vesicular stomatitis virus G-protein transport to the plasma membrane. The identification of PI4KIIIbeta as one of the PKD substrates should help to reveal the molecular events that enable transport-carrier formation.

摘要

蛋白激酶D（PKD）调节源自反式高尔基体网络的囊泡裂变。我们发现，磷脂酰肌醇4激酶IIIβ（PI4KIIIβ）——高尔基体复合体结构和功能中的关键因子——是PKD的生理底物。在三种PKD亚型中，只有PKD1和PKD2在一个从酵母到人类都高度保守的基序上使PI4KIIIβ磷酸化。PKD介导的磷酸化刺激了PI4KIIIβ的脂质激酶活性，并增强了水泡性口炎病毒G蛋白向质膜的转运。将PI4KIIIβ鉴定为PKD的底物之一，应有助于揭示促成运输载体形成的分子事件。

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Protein kinase D regulates vesicular transport by phosphorylating and activating phosphatidylinositol-4 kinase IIIbeta at the Golgi complex.蛋白激酶D通过在高尔基体复合体上磷酸化并激活磷脂酰肌醇-4激酶IIIβ来调节囊泡运输。
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2
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本文引用的文献

1
PKCeta is required for beta1gamma2/beta3gamma2- and PKD-mediated transport to the cell surface and the organization of the Golgi apparatus.β1γ2/β3γ2和PKD介导的向细胞表面运输以及高尔基体的组织需要PKCeta。
J Cell Biol. 2005 Apr 11;169(1):83-91. doi: 10.1083/jcb.200412089.
2
A rapid method for determining protein kinase phosphorylation specificity.一种用于确定蛋白激酶磷酸化特异性的快速方法。
Nat Methods. 2004 Oct;1(1):27-9. doi: 10.1038/nmeth708.
3
Activation of hematopoietic progenitor kinase 1 involves relocation, autophosphorylation, and transphosphorylation by protein kinase D1.造血祖细胞激酶1的激活涉及蛋白激酶D1介导的重新定位、自身磷酸化和转磷酸化。
Mol Cell Biol. 2005 Mar;25(6):2364-83. doi: 10.1128/MCB.25.6.2364-2383.2005.
4
A phosphorylation state-specific antibody recognizes Hsp27, a novel substrate of protein kinase D.一种磷酸化状态特异性抗体可识别热休克蛋白27（Hsp27），它是蛋白激酶D的一种新型底物。
J Biol Chem. 2005 Apr 15;280(15):15013-9. doi: 10.1074/jbc.C400575200. Epub 2005 Feb 22.
5
A plasma membrane pool of phosphatidylinositol 4-phosphate is generated by phosphatidylinositol 4-kinase type-III alpha: studies with the PH domains of the oxysterol binding protein and FAPP1.磷脂酰肌醇4-磷酸的质膜池由III型α磷脂酰肌醇4-激酶产生：用氧甾醇结合蛋白和FAPP1的PH结构域进行的研究。
Mol Biol Cell. 2005 Mar;16(3):1282-95. doi: 10.1091/mbc.e04-07-0578. Epub 2005 Jan 5.
6
Synthetic genetic array analysis of the PtdIns 4-kinase Pik1p identifies components in a Golgi-specific Ypt31/rab-GTPase signaling pathway.磷脂酰肌醇4-激酶Pik1p的合成基因阵列分析确定了高尔基体特异性Ypt31/rab-GTP酶信号通路中的组成成分。
Mol Biol Cell. 2005 Feb;16(2):776-93. doi: 10.1091/mbc.e04-08-0700. Epub 2004 Dec 1.
7
FAPPs control Golgi-to-cell-surface membrane traffic by binding to ARF and PtdIns(4)P.FAPPs通过与ARF和磷脂酰肌醇-4-磷酸（PtdIns(4)P）结合来控制从高尔基体到细胞表面的膜运输。
Nat Cell Biol. 2004 May;6(5):393-404. doi: 10.1038/ncb1119. Epub 2004 Apr 25.
8
Protein kinase Cdelta selectively regulates protein kinase D-dependent activation of NF-kappaB in oxidative stress signaling.蛋白激酶Cδ在氧化应激信号传导中选择性调节依赖蛋白激酶D的核因子κB激活。
Mol Cell Biol. 2004 Apr;24(7):2614-26. doi: 10.1128/MCB.24.7.2614-2626.2004.
9
Protein kinase D regulates basolateral membrane protein exit from trans-Golgi network.蛋白激酶D调节从反式高尔基体网络输出的基底外侧膜蛋白。
Nat Cell Biol. 2004 Feb;6(2):106-12. doi: 10.1038/ncb1090. Epub 2004 Jan 25.
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Protein kinase D-mediated anterograde membrane trafficking is required for fibroblast motility.成纤维细胞迁移需要蛋白激酶D介导的顺向膜运输。
Curr Biol. 2004 Jan 20;14(2):88-98. doi: 10.1016/j.cub.2004.01.003.