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本文引用的文献

1
WIP regulates persistence of cell migration and ruffle formation in both mesenchymal and amoeboid modes of motility.WIP 调节细胞迁移的持久性和片状伪足的形成，在间质和阿米巴样运动模式中都是如此。
PLoS One. 2013 Aug 7;8(8):e70364. doi: 10.1371/journal.pone.0070364. eCollection 2013.
2
Relaxation response induces temporal transcriptome changes in energy metabolism, insulin secretion and inflammatory pathways.松弛反应可引起能量代谢、胰岛素分泌和炎症途径中转录组的时相变化。
PLoS One. 2013 May 1;8(5):e62817. doi: 10.1371/journal.pone.0062817. Print 2013.
3
Disrupting the scaffold to improve focal adhesion kinase-targeted cancer therapeutics.破坏支架以改善黏着斑激酶靶向癌症治疗。
Sci Signal. 2013 Mar 26;6(268):pe10. doi: 10.1126/scisignal.2004021.
4
Assembly and disassembly of cell matrix adhesions.细胞基质黏附的组装与拆卸。
Curr Opin Cell Biol. 2012 Oct;24(5):569-81. doi: 10.1016/j.ceb.2012.06.010. Epub 2012 Jul 19.
5
Zyxin is a transforming growth factor-β (TGF-β)/Smad3 target gene that regulates lung cancer cell motility via integrin α5β1.锌指蛋白 217（Zyxin）是转化生长因子-β（TGF-β）/Smad3 的靶基因，通过整合素 α5β1 调节肺癌细胞的运动性。
J Biol Chem. 2012 Sep 7;287(37):31393-405. doi: 10.1074/jbc.M112.357624. Epub 2012 Jul 9.
6
Mechanotransduction in cells.细胞中的力学转导。
Cell Biol Int. 2012 Jun 1;36(6):567-70. doi: 10.1042/CBI20120071.
7
Mechanotransduction and focal adhesions.力学转导和黏着斑。
Cell Biol Int. 2012 Jul;36(7):649-52. doi: 10.1042/CBI20120184.
8
Tension is required but not sufficient for focal adhesion maturation without a stress fiber template.张力是形成焦点黏附成熟所必需的，但不是非应力纤维模板形成焦点黏附成熟的充分条件。
J Cell Biol. 2012 Feb 6;196(3):363-74. doi: 10.1083/jcb.201107042. Epub 2012 Jan 30.
9
The vinculin C-terminal hairpin mediates F-actin bundle formation, focal adhesion, and cell mechanical properties.衔接蛋白 C 端发夹结构域介导 F- 肌动蛋白束的形成、黏着斑的形成和细胞的力学特性。
J Biol Chem. 2011 Dec 30;286(52):45103-15. doi: 10.1074/jbc.M111.244293. Epub 2011 Nov 3.
10
A peptide derived from the Wiskott-Aldrich syndrome (WAS) protein-interacting protein (WIP) restores WAS protein level and actin cytoskeleton reorganization in lymphocytes from patients with WAS mutations that disrupt WIP binding.一种源自威特综合征蛋白相互作用蛋白（WIP）的肽可恢复 WIP 结合缺陷型 WAS 突变患者淋巴细胞中的 WAS 蛋白水平和肌动蛋白细胞骨架重组。
J Allergy Clin Immunol. 2011 Apr;127(4):998-1005.e1-2. doi: 10.1016/j.jaci.2011.01.015. Epub 2011 Mar 3.

WASP/N-WASP相互作用蛋白WIP与肌动蛋白的结合调节粘着斑组装和粘附。

Binding of the WASP/N-WASP-interacting protein WIP to actin regulates focal adhesion assembly and adhesion.

作者信息

Ramesh Narayanaswamy, Massaad Michel J, Kumar Lalit, Koduru Suresh, Sasahara Yoji, Anton Ines, Bhasin Manoj, Libermann Towia, Geha Raif

出版信息

Mol Cell Biol. 2014 Jul;34(14):2600-10. doi: 10.1128/MCB.00017-14.

DOI:10.1128/MCB.00017-14
PMID:24797074
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4097659/
Abstract

The actin cytoskeleton is essential for cell adhesion and migration, functions important for tumor invasion. In addition to binding N-WASP/WASP, WIP binds and stabilizes F-actin. WIP(-/-) fibroblasts were used to test the role of WIP in F-actin function. WIP(-/-) cells had defective focal adhesion (FA), stress fiber assembly, and adherence to substrates, functions that were restored by transduction of wild-type WIP. Protein and mRNA levels of several FA constituents regulated by the myocardin-related transcription factor (MRTF)–serum response factor (SRF) transcription factor complex were reduced in WIP(-/-) fibroblasts. The level of G-actin, which sequesters MRTF in the cytoplasm, was increased, and nuclear localization of MRTF-A and SRF was reduced, in WIP(-/-) fibroblasts. Transfection of an MRTF-A mutant that constitutively translocates to the nucleus or transfection of constitutively active SRF restored FA and stress fiber assembly. Fibroblasts from knock-in mice expressing a WIP mutant that fails to bind actin phenocopied WIP(-/-) fibroblasts. Thus, WIP is a novel regulator of FA assembly and cell adhesion.

摘要

肌动蛋白细胞骨架对于细胞黏附和迁移至关重要，而细胞黏附和迁移是肿瘤侵袭的重要功能。除了结合N-WASP/WASP外，WIP还能结合并稳定F-肌动蛋白。利用WIP(-/-)成纤维细胞来测试WIP在F-肌动蛋白功能中的作用。WIP(-/-)细胞的粘着斑（FA）、应力纤维组装以及对底物的粘附存在缺陷，而转导野生型WIP可恢复这些功能。在WIP(-/-)成纤维细胞中，由心肌素相关转录因子（MRTF）-血清反应因子（SRF）转录因子复合物调控的几种FA成分的蛋白质和mRNA水平降低。在WIP(-/-)成纤维细胞中，将MRTF隔离在细胞质中的G-肌动蛋白水平升高，MRTF-A和SRF的核定位降低。转染组成型易位至细胞核的MRTF-A突变体或转染组成型活性SRF可恢复FA和应力纤维组装。表达无法结合肌动蛋白的WIP突变体的敲入小鼠的成纤维细胞表现出与WIP(-/-)成纤维细胞相似的表型。因此，WIP是FA组装和细胞黏附的新型调节因子。