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CLIC4 is a cytokinetic cleavage furrow protein that regulates cortical cytoskeleton stability during cell division

机译:CLIC4是一种细胞内切割呋喃,可调节细胞分裂期间皮质细胞骨架稳定性

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During mitotic cell division, the actomyosin cytoskeleton undergoes several dynamic changes that play key roles in progression through mitosis. Although the regulators of cytokinetic ring formation and contraction are well established, proteins that regulate cortical stability during anaphase and telophase have been understudied. Here, we describe a role for CLIC4 in regulating actin and actin regulators at the cortex and cytokinetic cleavage furrow during cytokinesis. We first describe CLIC4 as a new component of the cytokinetic cleavage furrow that is required for successful completion of mitotic cell division. We also demonstrate that CLIC4 regulates the remodeling of the sub-plasma-membrane actomyosin network within the furrow by recruiting MST4 kinase (also known as STK26) and regulating ezrin phosphorylation. This work identifies and characterizes new molecular players involved in regulating cortex stiffness and blebbing during the late stages of cytokinetic furrowing.
机译:在有丝分裂细胞分裂期间,Actomyosin细胞骨架经历了几种动态变化,可通过有丝分裂进行进展中的关键作用。 虽然已经确定了细胞内环形成和收缩的调节剂,但已经被描述了调节内源和Telophase期间皮质稳定性的蛋白质。 在这里,我们描述了Clic4在Cortex和细胞因子因不能因子因不能在细胞因子期间调节肌动蛋白和肌动蛋白调节剂的作用。 我们首先将Clic4描述为成功完成有丝分裂细胞划分所需的细胞因激裂解沟的新组分。 我们还证明CLIC4通过募集MST4激酶(也称为STK26)并调节ezrin磷酸化来调节斑血管膜肌素网络的重塑。 这项工作识别并表征新的分子参与在细胞因子发作沟的后期调节皮质僵硬和膨胀的新分子器。

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