Clark Kristopher, Langeslag Michiel, Figdor Carl G, van Leeuwen Frank N
Department of Tumor Immunology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, PO Box 9101, 6500 HB Nijmegen, The Netherlands.
Trends Cell Biol. 2007 Apr;17(4):178-86. doi: 10.1016/j.tcb.2007.02.002. Epub 2007 Feb 21.
Adherent cells respond to mechanical properties of the surrounding extracellular matrix. Mechanical forces, sensed at specialized cell-matrix adhesion sites, promote actomyosin-based contraction within the cell. By manipulating matrix rigidity and adhesion strength, new roles for actomyosin contractility in the regulation of basic cellular functions, including cell proliferation, migration and stem cell differentiation, have recently been discovered. These investigations demonstrate that a balance of forces between cell adhesion on the outside and myosin II-based contractility on the inside of the cell controls many aspects of cell behavior. Disturbing this balance contributes to the pathogenesis of various human diseases. Therefore, elaborate signaling networks have evolved that modulate myosin II activity to maintain tensional homeostasis. These include signaling pathways that regulate myosin light chain phosphorylation as well as myosin II heavy chain interactions.
贴壁细胞对周围细胞外基质的力学特性作出反应。在特殊的细胞-基质粘附位点感知到的机械力会促进细胞内基于肌动球蛋白的收缩。通过操纵基质硬度和粘附强度，最近发现了肌动球蛋白收缩性在调节包括细胞增殖、迁移和干细胞分化在内的基本细胞功能中的新作用。这些研究表明，细胞外部的粘附力与细胞内部基于肌球蛋白II的收缩力之间的平衡控制着细胞行为的许多方面。打破这种平衡会导致各种人类疾病的发病机制。因此，已经进化出了复杂的信号网络来调节肌球蛋白II的活性以维持张力稳态。这些包括调节肌球蛋白轻链磷酸化以及肌球蛋白II重链相互作用的信号通路。
