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首页> 外文期刊>ACS Macro Letters >F-Actin Fragmentation Induces Distinct Mechanisms of Stress Relaxation in the Actin Cytoskeleton
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F-Actin Fragmentation Induces Distinct Mechanisms of Stress Relaxation in the Actin Cytoskeleton

机译:F-肌动蛋白片段化诱导肌动蛋白细胞骨架中应力松弛的不同机制。

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摘要

The diverse mechanical properties of the F-actin cytoskeleton mediate essential physical behaviors of the cells, including cell division, migration, and shape change. These properties include strain stiffening and stress relaxation that limit cell shape change and determine its rate. To date, stress relaxation has been mainly attributed to the transient nature of cross-linkers that connect F-actins. By contrast, the potential impacts of rich F-actin dynamics to the stress relaxation have been neglected in most previous studies. Thus, in this study, we use a novel computational model to demonstrate that F-actin severing arising from compression-induced filament buckling coordinates with cross-linker unbinding, leading to very distinct modes of stress relaxation. Furthermore, we establish the conditions under which the F-actin severing dominates the mechanical response, providing additional mechanistic insight into the viscoelasticity of the F-actin cytoskeleton.
机译:F-肌动蛋白细胞骨架的各种机械特性介导了细胞的基本物理行为,包括细胞分裂,迁移和形状变化。这些特性包括应变硬化和应力松弛,它们限制了单元形状的变化并决定了其速率。迄今为止,应力松弛主要归因于连接F-肌动蛋白的交联剂的瞬时性质。相比之下,以前的大多数研究都忽略了丰富的F-肌动蛋白动力学对应力松弛的潜在影响。因此,在这项研究中,我们使用一种新颖的计算模型来证明由压缩诱导的细丝屈曲引起的F-肌动蛋白切断与交联剂解键配合,从而导致非常不同的应力松弛模式。此外,我们建立了F-肌动蛋白切断主导机械反应的条件,从而为F-肌动蛋白细胞骨架的粘弹性提供了更多的力学见解。

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