环磷酸腺苷/蛋白激酶A对基于肌动蛋白的细胞迁移的调控

Regulation of actin-based cell migration by cAMP/PKA.

作者信息

Howe Alan K

机构信息

Department of Pharmacology, Vermont Cancer Center, University of Vermont, HSRF# 322, Burlington 05405-0075, USA.

出版信息

Biochim Biophys Acta. 2004 Jul 5;1692(2-3):159-74. doi: 10.1016/j.bbamcr.2004.03.005.

Abstract

A wide variety of soluble signaling substances utilize the cyclic AMP-dependent protein kinase (PKA) pathway to regulate cellular behaviors including intermediary metabolism, ion channel conductivity, and transcription. A growing literature suggests that integrin-mediated cell adhesion may also utilize PKA to modulate adhesion-associated events such as actin cytoskeletal dynamics and migration. PKA is dynamically regulated by integrin-mediated cell adhesion to extracellular matrix (ECM). Furthermore, while some hallmarks of cell migration and cytoskeletal organization require PKA activity (e.g. activation of Rac and Cdc42; actin filament assembly), others are inhibited by it (e.g. activation of Rho and PAK; interaction of VASP with the c-Abl tyrosine kinase). Also, cell migration and invasion can be impeded by either inhibition or hyper-activation of PKA. Finally, a number of A-kinase anchoring proteins (AKAPs) serve to associate PKA with various components of the actin cytoskeleton, thereby enhancing and/or specifying cAMP/PKA signaling in those regions. This review discusses the growing literature that supports the hypothesis that PKA plays a central role in cytoskeletal regulation and cell migration.

摘要

多种可溶性信号物质利用环磷酸腺苷依赖性蛋白激酶(PKA)途径来调节细胞行为,包括中间代谢、离子通道传导性和转录。越来越多的文献表明,整合素介导的细胞黏附也可能利用PKA来调节与黏附相关的事件,如肌动蛋白细胞骨架动力学和迁移。PKA受整合素介导的细胞与细胞外基质(ECM)黏附的动态调节。此外,虽然细胞迁移和细胞骨架组织的一些特征需要PKA活性(例如Rac和Cdc42的激活;肌动蛋白丝组装),但其他特征则受到其抑制(例如Rho和PAK的激活;VASP与c-Abl酪氨酸激酶的相互作用)。同样,PKA的抑制或过度激活都可能阻碍细胞迁移和侵袭。最后,一些A激酶锚定蛋白(AKAPs)可使PKA与肌动蛋白细胞骨架的各种成分结合,从而增强和/或在这些区域特异性调节环磷酸腺苷/蛋白激酶A信号传导。本文综述了越来越多支持PKA在细胞骨架调节和细胞迁移中起核心作用这一假说的文献。

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