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极光激酶A在高尔基体依赖性有丝分裂进入调控中的作用。

The role of Aurora-A kinase in the Golgi-dependent control of mitotic entry.

作者信息

Cervigni Romina Ines, Barretta Maria Luisa, Persico Angela, Corda Daniela, Colanzi Antonino

机构信息

Institute of Protein Biochemistry; Naples, Italy.

出版信息

Bioarchitecture. 2011 Mar;1(2):61-65. doi: 10.4161/bioa.1.2.15329.

DOI:10.4161/bioa.1.2.15329
PMID:21866264
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3158628/
Abstract

During mitosis, the Golgi complex undergoes a multi-step fragmentation process that is instrumental to its correct partitioning into the daughter cells. To prepare for this segregation, the Golgi ribbon is initially separated into individual stacks during the G2 phase of the cell cycle. Then, at the onset of mitosis, these individual stacks are further disassembled into dispersed fragments. Inhibition of this Golgi fragmentation step results in a block or delay of G2/M transition, depending on the experimental approach. Thus, correct segregation of the Golgi complex appears to be monitored by a 'Golgi mitotic checkpoint'. Using a microinjection-based approach, we recently identified the first target of the Golgi checkpoint, whereby a block of this Golgi fragmentation impairs recruitment of the mitotic kinase Aurora-A to, and its activation at, the centrosomes. Overexpression of Aurora-A can override this cell cycle block, indicating that Aurora-A is a major effector of the Golgi checkpoint. We have also shown that this block of Aurora-A recruitment to the centrosomes is not mediated by the known mechanisms of regulation of Aurora-A function. Here we discuss our findings in relation to the known functions of Aurora-A.

摘要

在有丝分裂期间,高尔基体复合体经历一个多步骤的碎片化过程,这对于其正确分配到子细胞中至关重要。为了准备这种分离,高尔基体带在细胞周期的G2期最初被分离成单个的堆叠。然后,在有丝分裂开始时,这些单个的堆叠进一步分解成分散的片段。抑制这个高尔基体碎片化步骤会导致G2/M转换的阻滞或延迟,这取决于实验方法。因此,高尔基体复合体的正确分离似乎受到一个“高尔基体有丝分裂检查点”的监测。使用基于显微注射的方法,我们最近确定了高尔基体检查点的第一个靶点,即这种高尔基体碎片化的阻滞会损害有丝分裂激酶Aurora-A向中心体的募集及其在中心体的激活。Aurora-A的过表达可以克服这种细胞周期阻滞,表明Aurora-A是高尔基体检查点的主要效应器。我们还表明,这种Aurora-A向中心体募集的阻滞不是由已知的Aurora-A功能调节机制介导的。在这里,我们讨论我们的发现与Aurora-A的已知功能的关系。

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本文引用的文献

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Shared and separate functions of polo-like kinases and aurora kinases in cancer.Polo-like 激酶和 Aurora 激酶在癌症中的共同和独立功能。
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Mitotic inhibition of GRASP65 organelle tethering involves Polo-like kinase 1 (PLK1) phosphorylation proximate to an internal PDZ ligand.GRASP65 细胞器连接的有丝分裂抑制涉及极向激酶 1(PLK1)在 PDZ 配体内部的临近磷酸化。
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Cdk1 activity is required for mitotic activation of aurora A during G2/M transition of human cells.在人类细胞的G2/M期转换过程中,Cdk1活性是极光激酶A有丝分裂激活所必需的。
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