非肌肉肌球蛋白II调控在细胞迁移和分裂中的多重作用。

IF 11.4 1区 生物学 Q1 CELL BIOLOGY
Marina Garrido-Casado, Gloria Asensio-Juárez, Miguel Vicente-Manzanares
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引用次数: 24

摘要

非肌球蛋白II (NMII)是一种多聚体蛋白复合物,在真核细胞中产生大部分机械力。NMII功能有三个主要层次。第一级包括触发构象变化的事件,这些变化扩展了复合体,使其能够组装成细丝。第二个水平控制复合物的atp酶活性及其与延伸NMII细丝的微丝结合。第三层次包括调节细丝的稳定性和收缩性的事件。它们都协同工作,精细地控制细胞内产生的力。NMII是机械化学信号通路的一个常见终点,控制细胞对物理和化学细胞外信号的反应。特异性磷酸化以上下文依赖的方式调节NMII的激活。一些激酶以空间、时间和谱系限制的方式控制这些磷酸化,从而实现对细胞微环境的功能适应性。在这里,我们回顾了在细胞迁移和分裂的背景下控制NMII活性的机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Nonmuscle Myosin II Regulation Directs Its Multiple Roles in Cell Migration and Division.

Nonmuscle myosin II (NMII) is a multimeric protein complex that generates most mechanical force in eukaryotic cells. NMII function is controlled at three main levels. The first level includes events that trigger conformational changes that extend the complex to enable its assembly into filaments. The second level controls the ATPase activity of the complex and its binding to microfilaments in extended NMII filaments. The third level includes events that modulate the stability and contractility of the filaments. They all work in concert to finely control force generation inside cells. NMII is a common endpoint of mechanochemical signaling pathways that control cellular responses to physical and chemical extracellular cues. Specific phosphorylations modulate NMII activation in a context-dependent manner. A few kinases control these phosphorylations in a spatially, temporally, and lineage-restricted fashion, enabling functional adaptability to the cellular microenvironment. Here, we review mechanisms that control NMII activity in the context of cell migration and division.

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来源期刊
CiteScore
19.50
自引率
0.00%
发文量
21
期刊介绍: The Annual Review of Cell and Developmental Biology, established in 1985, comprehensively addresses major advancements in cell and developmental biology. Encompassing the structure, function, and organization of cells, as well as the development and evolution of cells in relation to both single and multicellular organisms, the journal explores models and tools of molecular biology. As of the current volume, the journal has transitioned from gated to open access through Annual Reviews' Subscribe to Open program, making all articles published under a CC BY license.
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