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本文引用的文献

1
The pro-apoptotic protein Par-4 facilitates vascular contractility by cytoskeletal targeting of ZIPK.促凋亡蛋白Par-4通过将ZIPK靶向细胞骨架来促进血管收缩性。
J Cell Mol Med. 2009 May;13(5):887-95. doi: 10.1111/j.1582-4934.2008.00374.x. Epub 2008 May 24.
2
ZIPK: a unique case of murine-specific divergence of a conserved vertebrate gene.ZIPK：脊椎动物保守基因鼠特异性分化的一个独特案例。
PLoS Genet. 2007 Oct;3(10):1884-93. doi: 10.1371/journal.pgen.0030180. Epub 2007 Sep 7.
3
ROCK1 phosphorylates and activates zipper-interacting protein kinase.ROCK1使拉链相互作用蛋白激酶磷酸化并激活该激酶。
J Biol Chem. 2007 Feb 16;282(7):4884-4893. doi: 10.1074/jbc.M609990200. Epub 2006 Dec 8.
4
Novel ZIP kinase isoform lacks leucine zipper.新型ZIP激酶亚型缺乏亮氨酸拉链。
Arch Biochem Biophys. 2006 Dec 15;456(2):194-203. doi: 10.1016/j.abb.2006.09.026. Epub 2006 Oct 16.
5
The death-associated protein kinases: structure, function, and beyond.死亡相关蛋白激酶：结构、功能及其他
Annu Rev Biochem. 2006;75:189-210. doi: 10.1146/annurev.biochem.75.103004.142615.
6
Phosphorylation of threonine-265 in Zipper-interacting protein kinase plays an important role in its activity and is induced by IL-6 family cytokines.拉链相互作用蛋白激酶中苏氨酸-265的磷酸化在其活性中起重要作用，且由白细胞介素-6家族细胞因子诱导产生。
Immunol Lett. 2006 Mar 15;103(2):127-34. doi: 10.1016/j.imlet.2005.10.015. Epub 2005 Nov 9.
7
Par-4-mediated recruitment of Amida to the actin cytoskeleton leads to the induction of apoptosis.Par-4介导的Amida向肌动蛋白细胞骨架的募集导致细胞凋亡的诱导。
Exp Cell Res. 2005 Dec 10;311(2):177-91. doi: 10.1016/j.yexcr.2005.09.010. Epub 2005 Oct 14.
8
Binding and phosphorylation of par-4 by akt is essential for cancer cell survival.Akt对par-4的结合和磷酸化作用对于癌细胞存活至关重要。
Mol Cell. 2005 Oct 7;20(1):33-44. doi: 10.1016/j.molcel.2005.08.016.
9
Direct binding to ceramide activates protein kinase Czeta before the formation of a pro-apoptotic complex with PAR-4 in differentiating stem cells.在分化的干细胞中，与神经酰胺的直接结合在与PAR-4形成促凋亡复合物之前激活蛋白激酶Czeta。
J Biol Chem. 2005 Jul 15;280(28):26415-24. doi: 10.1074/jbc.M501492200. Epub 2005 May 18.
10
Binding of Par-4 to the actin cytoskeleton is essential for Par-4/Dlk-mediated apoptosis.Par-4与肌动蛋白细胞骨架的结合对于Par-4/Dlk介导的细胞凋亡至关重要。
Exp Cell Res. 2005 May 1;305(2):392-408. doi: 10.1016/j.yexcr.2005.01.012.

在Dlk/Par-4介导的细胞凋亡中，Par-4是死亡相关蛋白样激酶（Dlk）的一个重要下游靶点。

Par-4 is an essential downstream target of DAP-like kinase (Dlk) in Dlk/Par-4-mediated apoptosis.

作者信息

Boosen Meike, Vetterkind Susanne, Kubicek Jan, Scheidtmann Karl-Heinz, Illenberger Susanne, Preuss Ute

机构信息

Institute of Genetics, University of Bonn, D-53117 Bonn, Germany.

出版信息

Mol Biol Cell. 2009 Sep;20(18):4010-20. doi: 10.1091/mbc.e09-02-0173. Epub 2009 Jul 22.

DOI:10.1091/mbc.e09-02-0173
PMID:19625447
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2743620/
Abstract

Prostate apoptosis response-4 (Par-4) was initially identified as a gene product up-regulated in prostate cancer cells undergoing apoptosis. In rat fibroblasts, coexpression of Par-4 and its interaction partner DAP-like kinase (Dlk, which is also known as zipper-interacting protein kinase [ZIPK]) induces relocation of the kinase from the nucleus to the actin filament system, followed by extensive myosin light chain (MLC) phosphorylation and induction of apoptosis. Our analyses show that the synergistic proapoptotic effect of Dlk/Par-4 complexes is abrogated when either Dlk/Par-4 interaction or Dlk kinase activity is impaired. In vitro phosphorylation assays employing Dlk and Par-4 phosphorylation mutants carrying alanine substitutions for residues S154, T155, S220, or S249, respectively, identified T155 as the major Par-4 phosphorylation site of Dlk. Coexpression experiments in REF52.2 cells revealed that phosphorylation of Par-4 at T155 by Dlk was essential for apoptosis induction in vivo. In the presence of the Par-4 T155A mutant Dlk was partially recruited to actin filaments but resided mainly in the nucleus. Consequently, apoptosis was not induced in Dlk/Par-4 T155A-expressing cells. In vivo phosphorylation of Par-4 at T155 was demonstrated with a phospho-specific Par-4 antibody. Our results demonstrate that Dlk-mediated phosphorylation of Par-4 at T155 is a crucial event in Dlk/Par-4-induced apoptosis.

摘要

前列腺凋亡反应蛋白4（Par-4）最初被鉴定为在经历凋亡的前列腺癌细胞中上调的一种基因产物。在大鼠成纤维细胞中，Par-4与其相互作用伴侣DAP样激酶（Dlk，也称为拉链相互作用蛋白激酶[ZIPK]）的共表达会诱导该激酶从细胞核重新定位到肌动蛋白丝系统，随后是广泛的肌球蛋白轻链（MLC）磷酸化并诱导凋亡。我们的分析表明，当Dlk/Par-4相互作用或Dlk激酶活性受损时，Dlk/Par-4复合物的协同促凋亡作用会被消除。分别使用携带丙氨酸替代残基S154、T155、S220或S249的Dlk和Par-4磷酸化突变体进行的体外磷酸化测定，确定T155是Dlk的主要Par-4磷酸化位点。在REF52.2细胞中的共表达实验表明，Dlk在T155位点对Par-4的磷酸化对于体内凋亡诱导至关重要。在存在Par-4 T155A突变体的情况下，Dlk部分被募集到肌动蛋白丝，但主要位于细胞核中。因此，在表达Dlk/Par-4 T155A的细胞中未诱导凋亡。使用磷酸化特异性Par-4抗体证明了Par-4在T155位点的体内磷酸化。我们的结果表明，Dlk介导的Par-4在T155位点的磷酸化是Dlk/Par-4诱导凋亡中的关键事件。